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Ebbattth 

Page  75,  Figure  shown  is  not  the  Brown  sphyg- 
momanometer described  in  the  text,  but  the  Baum- 
anometer  manufactured  by  W.  A.  Baum  Co.,  Inc., 
New  York.  It  is  claimed  that  the  Baumanometer 
is  made  with  particular  care  and  hence  the  readings 
are  said  to  be  more  accurate  than  other  mercury 
instruments.  It  is  apparently  a  good  instrument. 
The  author  has  had  no  personal  experience  with  it. 


ARTERIOSCLEROSIS 

AND 

HYPERTENSION 


With  Chapters  on  Blood  Pressure 


BY 

LOUIS  M.  WARFIELD,  A.B.,  M.D.,  (Johns  Hopkins), 

F.A.C.P. 

FORMERLY   PROFESSOR    OF    CLINICAL    MEDICINE,    MARQUETTE    UNIVERSITY    MEDICAL 
SCHOOL;   CHIEF  PHYSICIAN  TO  MILWAUKEE  COUNTY  HOSPITAL;   ASSOCIATE 
MEMBER  ASSOCIATION   AMERICAN  PHYSICIANS;    MEMBER  AMERI- 
CAN  ASSOCIATION   PATHOLOGISTS   AND    BACTERIOLOGISTS; 
AMERICAN  MEDICAL  ASSOCIATION,  ETC.,  FELLOW 
AMERICAN  COLLEGE  OF  PHYSICIANS 


THIRD  EDITION 


ST.  LOUIS 

C.  V.  MOSBY  COMPANY 

1920 


Copyright,  1912,  1920,  by  C.  V.  Mosby  Company 


Press    of 

C.    V.    Mosby   Comj^any 

St.    Louis 


TO 

MY  MOTHER 

THIS   VOLTTME   IS    AFFECTIOXATELY 
DEDICATED 


1102676 


PKEFACE  TO  THIRD  EDITIOX 

Several  years  have  elapsed  since  the  appearance  of  the 
second  edition  of  this  book.  During  this  time  there  has 
been  considerable  experimentation  and  much  writing  on 
arteriosclerosis.  The  total  of  all  work  has  not  been  to  add 
very  much  to  our  knowledge  of  the  etiology  of  arterial  de- 
generation. Points  of  view  and  opinions  change  from  time 
to  time.  It  is  so  with  arteriosclerosis.  In  this  edition  ar- 
teriosclerosis is  not  regarded  as  a  disease  with  a  definite 
etiologic  factor.  Rather  it  is  looked  upon  as  a  degenerative 
process  affecting  the  arteries  following  a  variety  of  causes 
more  or  less  ill  defined.  It  is  not  considered  a  true  disease. 
Possibly  syphilitic  arteritis  may  be  viewed  as  an  entity,  the 
cause  is  known  and  the  lesions  are  characteristic. 

Much  new  material  and  many  new  figures  have  been 
added  to  this  edition.  Some  rearranging  has  been  done. 
The  chapter  on  Blood  Pressure  has  been  much  expanded 
and  some  original  observations  have  been  included.  The 
literature  has  been  selected  rather  than  indiscriminately 
quoted.  Much  that  is  written  on  the  suljject  is  of  little 
value. 

It  has  always  seemed  to  the  author  that  there  is  not 
enough  of  the  personal  element  in  medical  writings.  At  the 
risk  of  being  severely  criticized,  lie  has  attemj)ted  to  make 
this  book  represent  largely  his  own  ideas,  only  here  and 
there  quoting  from  the  literature. 

New"  chapters  on  Cardiac  Irregularities  Associated  with 
Arteriosclerosis,  and  Blood  Pressure  in  Its  Clinical  Appli- 
cation have  been  added. 

The  fact  that  the  book  lias  passed  through  two  editions  is 
very  gratifying  and  seems  to  show  that  it  has  met  with  fa- 
vor. The  author  takes  this  opportunity  of  thanking  those 
who  have  loaned  hiin  illustrations.  AVherever  figures  are 
borrowed  due  credit  is  given. 

15 


16  PREFACE 

It  is  hoped  that  tlie  kind  ol*  reception  accorded  to  the  first 
and  second  editions  will  also  not  he  Avitlihcld  from  this  pres- 
ent edition. 

Louis  M.  AVarfield. 

Mihvaiikeo,  Wise. 


PREFACE  TO  THE  SECOND  EDITION 

In  this  second  edition  so  many  changes  and  additions 
have  been  made  that  the  book  is  practically  a  new  one.  All 
the  chapters  which  were  in  the  previous  edition  have  been 
carefully  revised.  Two  chapters, ' '  Pathology ' '  and  ' '  Phys- 
iology," have  been  completely  rewritten  and  brought  up  to 
date.  It  was  thought  best  to  add  some  references  for  those 
who  had  interest  enough  to  pursue  the  subject  further. 
These  references  have  been  selected  on  account  of  the  read- 
iness with  Avhicli  they  may  be  procured  in  any  library,  public 
or  private.  Two  new  chaj)ters  have  been  added — one  on 
"The  Physical  Examination  of  the  Heart  and  Arteries," 
the  other  on  "Arteriosclerosis  in  Its  Relation  to  Life  In- 
surance," and  it  is  hoped  that  these  will  add  to  the  prac- 
tical value  of  the  book. 

Arteriosclerosis  can  scarcely  be  considered  apart  from 
blood  pressure,  and  in  the  view  expressed  within,  with 
which  some  may  not  concur,  high  tension  is  considered  to  be 
a  large  factor  in  the  production  of  arteriosclerosis.  As  the 
data  on  blood  pressure  have  increased,  the  importance  of  it 
has  become  more  evident.  The  chapter  on  "Blood  Pres- 
sure" has  been  Avholly  rewritten,  expanded  so  as  to  give 
a  comprehensive  grasp  of  the  essential  features,  and  several 
illustrations  have  l)een  added  in  order  to  elucidate  the  text 
more  fully.  The  chief  objects  in  view  Avere  to  make  clear 
to  the  physician  the  teclinicpie  and  the  necessity  for  estimat- 
ing both  systolic  and  diastolic  pressures. 

The  author  is  grateful  for  the  kindly  reception  accorded 
the  first  edition.    No  one  is  more  keenly  aware  of  the  im- 


PREFACE  17 

perfections  than  he.  The  necessity  for  a  second  edition  is 
taken  to  mean  that  the  book  has  found  a  jDhice  for  itself 
and  has  been  of  use  to  some. 

The  author  hopes  that  this  new  edition  will  fulfill  ade- 
quately the  purpose  for  which  he  j)repared  the  book — 
namely,  as  a  practical  guide  to  the  knowledge  and  ajopre- 
ciation  of  a  most  important  and  exceedingly  common 
disease. 

Louis  M.  AVarfield. 

Milwaukee,  May,  1912. 


PREFACE  TO  THE  FIRST  EDITION 

It  is  hoped  that  this  small  volume  may  fill  a  want  in  the 
already  crowded  field  of  medical  monographs.  The  au- 
thor has  endeavored  to  give  to  the  general  practitioner  a 
readable,  authoritative  essay  on  a  disease  which  is  espe- 
cially an  outcome  of  modern  civilization.  To  that  end  all 
the  available  literature  has  been  freely  consulted,  and  the 
newest  results  of  experimental  research  and  the  recent 
ideas  of  leading  clinicians  have  been  summarized.  The  au- 
thor has  supplemented  these  with  results  from  his  own 
experience,  but  has  thought  it  best  not  to  burden  the  con- 
tents with  case  histories. 

The  stress  and  strain  of  our  daily  life  has,  as  one  of 
its  consequences,  early  arterial  degeneration.  There  can 
be  no  doubt  that  arterial  disease  in  the  comparatively 
young  is  more  frequent  than  it  was  twenty-five  years  ago, 
and  that  the  mortalitj^  from  diseases  directly  dependent 
on  arteriosclerotic  changes  is  increasing.  Fortunately,  the 
almost  universal  habit  of  getting  out  of  doors  whenever 
possible,  and  the  revival  of  interest  in  athletics  for  persons 
of  all  ages,  have  to  some  extent  counteracted  the  tendency 
to  early  decay.  Nevertheless,  the  actual  average  pro- 
longation of  life  is  more  probably  due  to  the  very  great 
reduction  in  infant  mortality  and  in  deaths  from  infectious 
and  communicable  diseases. 


18  PREFACE 

The  wear  and  tear  on  the  liunian  organism  in  our  mod- 
ern Avay  of  living  is  excessive.  Hard  work,  worry,  and 
liigli  living  all  predispose  to  degenerative  changes  in  the 
arteries,  and  so  bring  on  premature  old  age.  The  author 
has  tried  to  emphasize  this  by  laying  stress  on  the  preven- 
tion of  arteriosclerosis  rather  than  on  the  treatment  of  the 
fully  developed  disease. 

Xo  bibliography  is  given,  as  this  is  not  intended  as  a 
reference  book,  but  rather  as  a  guide  to  a  better  apprecia- 
tion and  understanding  of  a  most  important  subject.  It 
has  been  difficult  to  keep  from  wandering  off  into  full  dis- 
cussions of  conditions  incident  to  and  accompanied  by 
arteriosclerosis,  but,  in  order  to  be  clear  in  his  statements 
and  complete  in  his  descri]3tions,  the  author  has  to  invade 
the  fields  of  heart  disease,  kidney  disease,  brain  disease, 
etc.  It  is  hoped,  however,  that  these  excursions  will  serve 
to  show  how  intimately  disease  of  the  arteries  is  bound 
up  with  diseases  of  all  the  organs  and  tissues  of  the  body. 

Some  autlioi"S  have  been  named  when  their  opinions 
have  been  given.  Thanks  are  extended  also  to  many  oth- 
ers to  whom  tlie  writer  is  indebted,  but  of  whom  no  indi- 
vidual mention  has  been  made. 

The  author  also  takes  this  opjDortunity  of  expressing 
his  appreciation  of  the  kindness  of  Dr.  I).  L.  Harris,  who 
took  the  microphotographs,  and  to  the  publishers  for  their 
unfailing  courtesy  and  consideration. 

Louis  M.  AVarfield. 

St.  Louis,  Aiifjust,  lilOS. 


CONTEXTS 


PAc;r, 
CHAPTER  I 

Anatomy 2.3 

Introduction,  25;  Definition,  26;  General  Structure  of  the  Arteries, 
27;  Arteries,  29;  Veins,  30;  Capillaries,  31. 

CHAPTER  II 

Pathology 32 

Syphilitic  Aortitis,  44 ;  Experimental  Arteriosclerosis,  50 ;  Arte- 
riosclerosis of  the  Pulmonary  Arteries,  63 ;  Sclerosis  of  the  Veins,  64. 

CHAPTER  III 

PnYSIOLOGY    OF    THE    CIRCULATION' Go 

Blood  Pressure,  68;  Blood  Pressure  Instruments,  70;  Technic,  80; 
Arterial  Pressure,  85;  Normal  Pressure  Variations,  88;  The  Aus- 
cultatory Blood  Pressure  Phenomenon,  90 ;  The  Maximum  and  Mini- 
mimi  Pressures,  94;  Relative  Importance  of  the  Systolic  and  Dia- 
stolic Pressures,  97;  Pulse  Pressure,  100;  Blood  Pressure  Variations, 
102;  Hypertension,  106;  Hypotension,  117;  The  Pulse,  123;  The 
Venous  Pulse,  123;  The  Electrocardiogram,  126. 

CHAPTER  IV 
Important  Cardiac  Irregularities  Associated  With  Arteriosclerosis     131 
Auricular    Flutter,    131 ;    Auricular   Fibrillation,    133 ;    A'entricular 
Fibrillation,  138;  Extrasystole,  138;  Heart  Block,  140. 

CHAPTER  V 

Blood  Pressure  in  Its  Clinical  Applications 147 

Blood  Pressure  in  Surgery,  147;  Head  Injuries,  148;  Shock  and 
Hemorrhage,  148;  Blood  Pressure  in  Obstetrics,  152;  Infectious 
Diseases,  153;  Valvular  Heart  Disease,  155;  Kidney  Disease,  155; 
Other  Diseases,  Liver,  Spleen,  Abdomen,  etc.,  156. 

CHAPTER  VI 

Etiology 157 

Congenital  Form,  157;  Acquired  Form,  159;  Hypertension,  159; 
Age,  Sex,  Race,  161;  Occupation,  162;  Food  Poisons,  163;  Infec- 
tious Diseases,  163;  Syphilis,  165;  Chronic  Drug  Intoxications,  166; 
Overeating,  167;  Mental  Strain,  168;  Muscular  Overwork,  169; 
Renal  Disease,  169;  Ductless  Glands,  171. 

19 


20  CONTENTS 

PAGE 

CHAPTER  VII 

The  Physical  Examination'  of  the  Heart  and  Arteries 172 

Heart  Bouiidarics,  172;  I'l'reiissioii,  174;  Auscultation,  17G;  Tlie 
Examination  of  tlie  Arteries,  177;  Estimation  of  Blood  Pressure, 
179;  Palpation,  ISO;  Pi'ecautious  When  Estimating  Blood  Pres- 
sure, 181;  The  \'alue  of  Blood  Pressure,  181. 

CHAPTER  VIII 

Symptoms  and  Physical  Signs ISr, 

General,  183;  Hypertension,  185;  The  Heart,  188;  Palpable  Arter- 
ies, 189;  Ocular  Signs  and  Symptoms,  190;  Xervous  Symptoms,  191. 

CHAPTER  IX 

Sy'mptoms  and  Physical  Signs 194 

Special,  194;  Cardiac,  19.j ;  Renal,  199;  Abdominal  or  Visceral,  201; 
Cerebral,  20.'5 ;  Spinal,  205;  Local  or  Peripheral,  207;  Pulmonary 
Artery,  209. 

CHAPTER  X 

Diagnosis 210 

Early  Diagnosis,  210;  Differential  Diagnosis,  215;  Diseases  in  Which 
Arteriosclerosis  is  Commonly  Found,  21G. 

CHAPTER  XI 
Prognosis 218 

CHAPTER  XII 
Prophylaxis 224 

CHAPTER  XIII 

Treatment 229 

Hygienic  Treatment,  2.'30 ;  Bahuothera])y,  233;  Personal  Haldts, 
234;  Dietetic  Treatment,  235;  Medicinal,  238;  Symptomatic  Treat- 
ment, 245. 

CHAPTER  XIV 
Arteriosclerosis  in  Its  Relation  to  Life  Insurance 249 

CHAPTER  XV 
Practical   Suggestions 256 


ILLUSTRATIONS 

I'lO.  PAGE 

1.  Cross   section   of   a   large   artery 28 

2.  Cross  section   of  a  coronary  artery 36 

3.  Arteriosclerosis  of  the  thoracic  and  alxTominal  aorta 39 

4.  Arteriosclerosis  of  the  arch  of  the  aorta 40 

5.  Normal  aorta 41 

G.  Eadiogram  shoAving  calcification  of  both  radial  and  ulnar  arteries     .  42 

7.  Syphilitic  aortitis  of  long  standing 44 

8.  Diagrammatic  representation  of   strain  hypertrophy 48 

9.  Strain  hypertrophy 49 

10.  Cross  section  of  small  artery  in  the  mesentery 56 

11.  Enormous   hypertrophy    of    left    ventricle 58 

12.  Aortic  incompetence  with  hypertrophy  and  dilatation  of  left  ventricle  61 

13.  Cook's  modification  of  Riva-Rocca's  blood  pressure  instrument     .     .  72 

14.  Stanton's   sphygmomanometer 73 

15.  The  Erlanger  sphygmomanometer  with  the  Hirschfelder  attachments  74 

16.  Desk  model  Baumanometer 75 

17.  Faught  blood  pressure  instrument 70 

18.  Rogers'    "Tycos"    dial   sphygmomanometer 77 

19.  Detail  of  the  dial  in  the  "Tycos"  instrument 78 

20.  Faught    dial    instrument 79 

21.  Detail  of  the   dial   of   the   Faught   instrument 79 

22.  The  Sanborn  instrument 80 

23.  Method  of  taking  blood  pressure  with  a  i)atient  in  sitting  position     .  81 

24.  Method  of  taking  blood  jjressuro  with  patient  lying  down     ....  82 

25.  Observation  by  tlie  auscultatory  method  and  a  mercury  instrument     .     84 

26.  Observation  by  the  auscultatory  method  and  a  dial  instrument     .     .  85 

27.  Schema  to  illustrate  decrease  in  pressure 86 

28.  Chart  showing  the  normal  limits  of  variation  in  systolic  blood  pressure  89 

29.  Tracing  of  auscultatory  phenomena 5*4 

30.  Tracing  of  auscultatory  phenomena     ...         ^5 

31.  Clinical  determination  of  diastolic  i)ressure,  fast  drum 96 

32.  Clinical  determination  of  diastolic  pressure,  slow  drum 9(> 

33.  Venous  blood  pressure  instrument       121 

34.  New    venous    i^ressure    instrument        122 

35.  Events  in  the  cardiac  cycle 1-^ 

36.  Simultaneous  tracings  of  the  jugular  and  carotid  i)ulses     .     .     .     .  125 

37.  Jugular  and  carotid  tracings l--^ 

38.  Right  side  of  the  heart  showing  distribution  of  the  two  vagus  nerves  127 

39.  Normal    electrocardiogram 1-8 

40.  Auricular  flutter 132 

41.  Auricular   fibrillation ^^^ 

21 


22  ILLUSTRATIONS 

i^l«.  P.UiH 

42.  Auricular   fibrillation i;i4 

4:i.  Pulse    deficit i;{.3 

44.  Veiitrieular  fibrillation TAJ 

45.  Auricular    pxtrasystoles ];{<) 

4().  A'ontricular   cxtrasystolc i;;9 

47.  Delayed  conduction 141 

48.  Partial    lieart    block        141 

4 SI.  Complete   heart   block 142 

"lO.  Alternating  periods  of  sinus  rhythm  and  auriculoventricular  rliytluu  144 

51.  Auriculoventricular    or    "nodal"    rhythm 144 

52.  Influence  of  mechanical  pressure  on  the  right  vagus  nerve     .     .     .     .  144 
C>'A.   Schematic  distribution  of  right  and  left  vagus 145 

54.  Blood  pressure  record  from  a  normal  reaction  to  ether 149 

55.  Chart    showing  the   method   of   recording   blood   pressure    during    an 

operation 150 

56.  Method  of  using  blood  pressure  instrument  during  operation     .     .     .  151 

57.  Finger-til)  palpation  of  the  radial  artery 178 

58.  Finger-tip  palpation  of  the  radial  artery 178 

59.  Aneurysm    of    the    heart    wall 1!*<3 

60.  Large  aneurysm  of  the  aorta  eroding  the  sternum It'S 


ARTERIOSCLEROSIS  AND  HYPERTENSION 


CHAPTER  I 
ANATOMY 


With  the  increased  complexity  of  our  modern  life  comes 
increased  wear  and  tear  on  the  human  organism.  ''A  man 
is  as  old  as  his  arteries"  is  an  old  dictum,  and,  like  many 
proverbs,  the  application  to  mankind  today  is,  if  any- 
thing, more  pertinent  than  it  was  when  the  saying  was 
first  uttered.  Notwithstanding  the  fact  that  the  average 
age  of  mankind  at  death  has  been  materially  lengthened — 
the  increase  in  years  amounting  to  fourteen  in  the  past 
one  hundred  years  of  history — clinicians  and  pathologists 
are  agreed  that  the  arterial  degeneration  known  as  arterio- 
sclerosis is  present  to  an  alarming  extent  in  persons  over 
forty  years  of  age.  Figures  in  all  vital  statistics  have  shown 
us  that  all  affections  of  the  circulatory  and  renal  s^'stems 
are  definitely  on  the  increase.  ''Arterial  diseases  of  va- 
rious kinds,  atheroma,  aneurysm,  etc.,  caused  15,685  deaths 
in  1915,  or  23.3  per  100,000.  This  rate,  although  somewhat 
lower  than  the  corresponding  ones  for  1912  and  1913,  is 
higher  than  that  for  1914,  and  is  very  much  higher  than 
that  for  1900,  which  was  6.1." 

The  great  group  of  cases  of  which  cardiac  incompetence, 
aneurysm,  cerebral  apoplexy,  chronic  nephritis,  emphysema, 
and  chronic  bronchitis  are  the  most  frequent  and  important 
appear  as  terminal  events  in  which  arteriosclerosis  has 
probably  played  an  important  part. 

Thus,  in  the  sense  in  which  we  speak  of  tuberculosis  or 
pneumonia  as  a  distinct  disease,  we  can  not  so  designate  the 
diseased  condition  of  the  arteries. 

Arteriosclerosis  is  not  a  disease  sui  generis.     It  is  best 

25 


2G  AllTETUOSCLEROSFS 

viewed  as  a  det>-eiieration  of  the  coats  of  the  arteries,  both 
large  and  small  resulting  in  several  different  more  or  less 
distinct  types. 

These  tyi)es  blend  one  into  tlie  other  and  in  the  same  pa- 
tient all  types  may  be  found.  Thus  the  sclerosis  of  the 
arteries  is  tlie  result  of  a  variety  of  causes,  none  of  wliich 
is  definitely  known  in  the  sense  of  a  bacterial  disease.  As 
we  shall  see  later,  one  type  of  arteriosclerosis  has  a  special 
pathology  and  etiology,  the  syphilitic  arterial  changes. 

Bearing  in  mind  that  arteriosclerosis  (called  by  some 
''arteriocapillary  fibrosis,"  by  others  '' atherosclerosis") 
is  not  a  true  disease,  it  may,  for  convenience  be  defined  as  a 
chronic  disease  of  the  arteries  and  arterioles,  characterized 
anatomically  by  increase  or  decrease  of  the  thickness  of  the 
walls  of  the  blood  vessels,  the  initial  lesion  being  a  weak- 
ening of  the  middle  layer  caused  by  various  toxic  or  me- 
chanical agencies.  This  weakness  of  the  media  leads  to 
secondary  effects,  which  include  hypertrophy  or  atrophy 
of  the  inner  layer — and  not  infre(|uently  hypertrophy  of 
the  outer  layer — connective  tissue  formation  and  calcifi- 
cation in  the  vessels,  and  the  formation  of  minute  aneu- 
rysms along  them.  The  term  arteriocapillary  fibrosis  has 
a  ])roader  meaning,  but  is  a  cumbersome  phrase,  and  con- 
veys the  idea  that  the  capillary  changes  are  an  essential 
feature  of  the  process,  whereas  these  are  for  the  most  part 
secondary  to  the  changes  in  the  arteries.  The  veins  do 
not  always  esca])e  in  the  general  morbid  process,  and  when 
these  are  atfected  the  whole  condition  is  sometimes  called 
vascular  sclerosis  or  angiosclerosis. 

Upon  the  anatomical  structure  of  the  arteries  depends, 
as  a  rule,  the  character  and  extent  of  the  arteriosclerotic 
lesions.  For  the  clear  comprehension  of  the  process,  it  is 
necessary  to  keep  in  mind  the  essential  histological  dif- 
ferences 1)etween  the  aorta  and  the  larger  and  smaller 
branches  of  the  arterial  tree. 

Tho  vascular  system  is  often  likened  to  a  central  pump, 
from  which  emanates  a  closed  system  of  tubes,  beginning 


AXATO^EY  27 

with  one  large  distributing  pipe,  wliicli  gives  rise  to  a  series 
of  tubes,  whose  num])er  is  constantly  increasing  at  the 
same  time  that  their  caliber  is  decreasing  in  size.  From 
the  smallest  of  these  tubes,  larger  and  larger  vessels  col- 
lect the  flowing  blood,  until,  at  the  pump,  two  large  trunks 
of  approximately  the  same  area  as  the  one  large  distribut- 
ing trunk  empty  the  blood  into  the  heart,  thus  completing 
the  circle.  This  is  but  a  rough  illustration,  and,  while  pos- 
sibly useful,  takes  into  account  none  of  the  vital  forces 
which  are  constantly  controlling  every  part  of  the  dis- 
tributing system. 

General  Structure  of  the  Arteries 

The  aorta  and  its  branches  are  highly  elastic  tubes,  hav- 
ing a  smooth,  glistening  inner  surface.  When  the  arteries 
are  cut  open,  they  present  a  yellowish  appearance,  due  to 
the  large  quantity  of  elastic  tissue  contained  in  the  walls. 
The  elasticity  is  practically  perfect,  being  both  longitudinal 
and  transverse.  The  essential  portion  of  any  blood  vessel 
is  the  endothelial  tube,  composed  of  flat  cells  cemented  to- 
gether by  intercellular  substance  and  having  no  stomata 
between  the  cells.  This  tube  is  reinforced  in  ditferent 
ways  by  connective  tissue,  smooth  muscle  fibers,  and  fibro- 
elastic  tissue.  Although  the  gradations  from  the  larger  to 
the  smaller  arteries  and  from  these  to  the  capillaries  and 
veins  are  almost  insensible,  yet  particular  arteries  pre- 
sent structural  characters  sufficiently  marked  to  achiiit  of 
histological  differentiation. 

The  whole  vascular  system,  including  the  heart,  has  an  en- 
dothelial lining,  which  may  constitute  a  distinct  inner  coat, 
the  tunica  intima,  or  may  be  without  coverings,  as  in  the 
case  of  the  capillaries.  The  intima  (Fig.  1 )  consists  typically 
of  endothelium,  reinforced  by  a  variable  amount  of  fibro- 
elastic  tissue,  in  which  the  elastic  fibers  predominate.  The 
tunica  media  is  composed  of  intermingled  bundles  of  elas- 
tic tissue,  smooth  muscle  fibers,  and  some  fibrous  tissue. 
The  adventitia  or  outer  coat  is  exceedingly  tough.     It  is 


28 


AUTEUIOSCLERO.SIS 


usually  thinner  than  the  media,  and  is  composed  of  fibro- 
elastic  tissue.  This  division  into  three  coats  is,  however, 
somewhat  arliitrary,  as  in  the  larger  arteries  particularly 
it  is  difficult  to  discover  any  distinct  separation  into  layers. 

The  muscular  layer  varies  from  single  scattered  cells,  in 
the  arterioles,  to  bands  of  fibers  making  up  the  body  of  the 
vessel  in  the  medium-sized  arteries  and  veins. 

There  is  elastic  tissue  in  all  but  the  smallest  arteries, 


l'*ig.  1. — Cross  section  of  a  large  arlery  sliowing  the  division  into  the  three  coats;  in- 
tinia,  media,  adventitia.  Tlie  intinia  is  a  thin  line  comjiosed  of  endothelial  cells.  The 
wavy  elastic  lamina  is  well  seen.  The  thick  middle  coat  is  composed  of  mnscle  fibers 
and  hl)roelastic  tissue.  The  loose  tissue  on  the  outer  (lower  portion  of  cut)  side  of  the 
media   is   the   adventitia.      (Microphotograph,    highly   magnified.) 

and  it  is  also  found  in  some  veins.  It  varies  in  amount 
from  a  loose  network  to  dense  membranes.  In  the  intima 
of  the  larger  arteries  the  elastic  tissue  occurs  as  sheets, 
which  under  the  microscope  appear  perforated  and  pitted, 
the  so-called  fenestrated  membrane  of  Henle. 

The  nutrient  vessels  of  the  arteries  and  veins,  the  vasa 
vasorum,  are  present  in  all  the  vessels  except  those  less 


AXATOMY  29 

tlian  one  millimeter  in  diameter.  The  vasa  vasorum  course 
in  the  external  coat  and  send  capillaries  into  the  media, 
supplying  the  outer  portion  of  the  coat  and  the  externa 
with  nutritive  material.  The  nutrition  of  the  intima  and 
inner  portion  of  the  media  is  obtained  from  the  blood  cir- 
culating through  the  vessel.  Lymphatics  and  nerves  are 
also  present  in  the  middle  and  outer  layers  of  the  vessels. 

Arteries 

The  structure  of  the  arteries  varies  notably,  depending 
upon  the  size  of  the  vessel.  A  cross  section  of  the  thoracic 
aorta  reveals  a  dense  netw'ork  of  elastic  fibers,  occupying 
practically  all  of  the  space  between  the  single  layer  of 
endothelial  cells  and  the  loose  elastic  and  connective  tis- 
sue network  of  the  outer  layer.  Smooth  muscle  fibers  are 
seen  in  the  middle  coat,  but,  in  comparison  with  the  mass 
of  elastic  tissue,  they  appear  to  have  only  a  limited  func- 
tion. 

In  a  cross  section  of  the  radial  artery  one  sees  a  wavy 
outline  of  intima,  caused  by  the  endothelium  following  the 
corrugations  of  the  elastica.  The  endothelium  is  seen  as 
a  delicate  line,  in  which  a  few  nuclei  are  visible.  The 
media  is  comparatively  thick,  and  is  composed  of  muscle 
cells,  arranged  in  flat  bundles,  and  plates  of  elastic  tissue. 
Between  the  media  and  the  externa  the  elastic  tissue  is 
somewhat  condensed  to  form  the  external  elastic  mem- 
brane. The  adventitia  varies  much  in  thickness,  being  bet- 
ter developed  in  the  medium-sized  than  in  the  large  arter- 
ies. It  is  composed  of  fibrous  tissue  mixed  with  elastic 
fibers. 

*' Followed  toward  the  capillaries,  the  coats  of  the  artery 
gradually  diminish  in  thickness,  the  endothelium  resting 
directly  upon  the  internal  elastic  membrane  so  long  as  the 
latter  persists,  and  afterward  on  the  rapidly  attenuating 
media.  The  elastica  becomes  progressively  reduced  until 
it  entirely  disappears  from  the  middle  coat,  which  then  be- 
comes a  purely  muscular  tunic,  and,  before  the  capillary  is 
reached,  is  reduced  to  a  single  layer  of  muscle  cells.     In 


?)0  AirrEllIOSCLEROSTS      ^ 

the  i^recapillary  arterioles  the  muscle  no  longer  forms  a 
continuous  layer,  l)ut  is  re])i"esente(l  l)y  groups  of  fiber  cells 
that  partially  wrap  around  the  vessel,  and  at  last  are  re- 
l)laced  by  isolated  elements.  After  the  disappearance  of 
the  muscle  cells  the  ])lood  vessel  has  become  a  true  capil- 
lary. The  adventitia  shares  in  the  general  reduction,  and 
gradually  diminishes  in  thickness  until,  in  the  smallest  ar- 
teries, it  consists  of  only  a  few  fibroelastic  strands  outside 
the  muscle  cells."     (Piersol's  Anatomy.) 

The  large  arteries  diifer  from  those  of  medium  size 
mainly  in  the  fact  that  there  is  no  sharp  line  of  demarca- 
tion between  the  intima  and  the  media.  There  is  also  much 
more  elastic  tissue  distributed  in  firm  bundles  throughout 
the  media,  and  there  are  fewer  muscle  fibers,  giving  a 
more  compact  appearance  to  the  artery  as  seen  in  cross 
section.  The  predominance  of  elastic  tissue  permits  of 
great  distention  by  the  blood  forced  into  the  artery  at 
every  heartbeat,  the  cali1)er  of  the  tube  being  less  markedly 
under  the  control  of  the  vasomotor  nerves  than  is  the  case 
in  the  small  arteries,  Avliere  the  muscle  tissue  is  relatively 
more  developed.  The  adventitia  of  the  large  arteries  is 
strong  and  firm,  and  is  made  up  of  interlacing  fil)roelastic 
tissue,  of  which  some  of  the  bundles  are  arranged  longi- 
tudinally. 

Veins 

The  walls  of  the  veins  are  thinner  than  those  of  the  ar- 
teries; they  contain  much  loss  elastic  and  muscular  tissue, 
and  are,  therefore,  more  flaccid  and  less  contractile.  ]\lany 
veins,  particularly  those  of  the  extremities,  are  provided 
with  cup-like  valves  opening  toward  the  heart.  These 
valves,  when  closed,  j^revent  the  return  of  the  blood  to  the 
periphery  and  distribute  the  static  pressure  of  the  blood 
column.  The  bulgings  caused  by  the  valves  may  be  seen 
in  the  superficial  veins  of  the  arm  and  leg.  There  are  no 
valves  in  the  veins  of  the  neck,  where  there  is  no  necessity 
for  such  a  protective  mechanism,  gravit}'  sufficing  to  drain 
the  venous  blood  from  the  cranial  cavitv. 


ANATOMY  31 

Capillaries 

These  arc  cnclotlielial  tubes  in  the  substance  of  the  or- 
gans, the  tissue  of  the  organ  giving  them  the  necessary 
support.  They  are  the  final  subdivisions  of  the  blood  ves- 
sels, and  the  vast  capillary  area  offers  the  greatest  amount 
of  resistance  to  the  blood  flow,  thus  serving  to  slow  the 
blood  stream  and  allowing  time  for  nutritive  substances 
or  waste  products  to  pass  from  and  to  the  blood.  I'sually 
the  capillaries  are  arranged  in  the  form  of  a  network, 
the  channels  in  any  one  tissue  being  of  nearly  uniform  size, 
and  the  closeness  of  the  mesh  depending  upon  the  organ. 

As  far  back  as  1865,  Strieker  observed  contraction  of  tlie 
capillaries.  This  observation  was  apj^arently  forgotten  un- 
til revived  again  by  Krogh  recently.  The  latter  finds  that 
the  capillaries  are  formed  of  cells  which  are  arranged  in 
strands  encircling  the  vessel.  The  capillaries  are  rarely 
longer  than  1  nun.,  and,  according  to  Krogh,  are  capable  of 
enormous  dilatation. 

The  rate  of  flow  through  any  capillary  area  is  very  incon- 
stant, and  the  usual  explanation  has  been  that  the  capilla- 
ries were  endothelial  tu])es  the  blood  flow  of  which  was  d(>- 
pendent  upon  the  contraction  or  dilatation  of  the  terminal 
arterioles.  The  actual  fact  that  in  an  observed  cajjillary 
area  some  capillaries  are  empty  renders  the  above  explana- 
tion untenable.  The  color  of  a  tissue  depends  upon  the  state 
of  filling  of  the  capillaries  with  blood. 

It  would  seem  that  all  the  evidence  now  leads  us  to  be- 
lieve that  the  capillaries  themselves  are  contractile  and  it 
is  even  possible  that  they  may  be  under  vasomotor  control. 
If  the  anatomic  structure  as  stated  above,  is  con-ect,  it 
would  take  but  a  slight  contraction  of  the  encircling  cell  to 
shut  off  comj)letely  the  capillary.  When  the  enormous  cap- 
illary bed  is  considered,  it  is  not  inconceival)le  that  circu- 
lating poisons  may  act  on  large  areas  and  produce  a  true 
capillary  resistance  to  the  onflow  of  blood  which  might 
express  itself,  if  long  continued,  in  actual  hypertroi)hy  of 
the  heart. 


CHAPTER  II 

PATHOLOGY 

The  whole  subject  of  the  pathology  of  arteriosclerosis  has 
been  much  enriched  by  the  study  of  the  experimental  lesions 
produced  by  various  drugs  and  microorganisms  upon  the 
aortas  of  rabbits.  Simple  atheroma  must  not  be  confused 
with  the  lesions  of  arteriosclerosis.  The  small  wdiitish  or 
yellowish  plaques  so  frequently  seen  on  the  aorta  and  its 
main  branches,  may  occur  at  any  age,  and  have  seemingly 
no  great  significance.  Such  plaques  may  grow  to  the  size 
of  a  dime  or  larger,  and  even  become  eroded.  They  repre- 
sent fatty  degeneration  of  the  intima  which,  at  times,  has 
no  demonstrable  cause;  at  times  follows  in  the  course  of 
various  diseases,  and  undoubtedly  is  due  to  disturbances  of 
nutrition  in  the  intima.  Except  for  the  remote  danger  of 
clot  formation  on  the  uneven  or  eroded  spot,  these  places 
are  of  no  special  significance,  and  are  not  to  be  confused 
with  the  atheroma  of  nodular  sclerosis. 

The  lesions  of  arteriosclerosis  are  of  a  different  char- 
acter. It  has  been  customary  to  differentiate  three  types: 
(1)  nodular;  (2)  diffuse;  (3)  senile.  It  must  be  understood 
that  this  is  not  a  classification  of  distinct  types.  As  a  rule 
in  advanced  arteriosclerosis,  lesions  representing  all  types 
and  all  grades  are  found.  The  nodular  type,  however,  may 
occur  in  the  aorta  alone,  the  branches  remaining  free.  This 
is  most  often  found  in  syphilitic  sclerosis  where  the  lesion  is 
confined  to  the  ascending  portion  of  the  arch  of  the  aorta. 

The  retrogressive  changes  of  advancing  years  can  not 
be  rightly  termed  disease,  yet  it  becomes  necessary  to  re- 
gard them  as  such,  for  the  senile  changes,  as  we  shall  see, 
may  be  but  the  advanced  stages  of  true  arteriosclerosis. 
Much  depends  on  the  nature  of  the  arterial  tissue  and  much 

32 


PATHOLOGY  33 

on  the  factors  at  work  tending  to  injure  the  tissue.  A  man 
of  forty  years  may  therefore  have  the  calcified,  pipe  stem 
arteries  of  a  man  of  eighty.  Our  parents  determine,  to 
great  extent,  the  kind  of  tissue  with  which  we  start  life. 
The  arteries  are  elastic  tubes  capable  of  much  stretching 
and  abuse.  In  the  aorta  and  large  branches  there  is  much 
elastic  tissue  and  relatively  little  muscle.  When  the  vessels 
have  reached  the  organs,  they  are  found  to  be  structurally 
changed  in  that  there  is  in  them  a  relatively  small  amount 
of  elastic  tissue  but  a  great  deal  of  smooth  muscle.  This 
is  a  provision  of  nature  to  increase  or  decrease  the  supply 
of  blood  at  any  point  or  points. 

The  aorta  and  the  large  branches  are  distributing  tubes 
only.  It  is  after  all  in  the  arterioles  and  smaller  arteries 
that  the  lesions  of  arteriosclerosis  do  the  most  damage.  A 
point  to  be  emphasized  is  that  the  whole  arterial  system  is 
rarely,  if  ever,  attacked  uniformly.  That  is,  there  may  be 
a  marked  degree  of  sclerosis  in  the  aorta  and  coronary 
arteries  with  very  little,  if  any,  change  in  the  radials.  On 
the  contrary,  a  few  peripheral  arteries  only  may  be  the  seat 
of  disease.  A  case  in  point  was  seen  at  autopsy  in  which 
the  aorta  in  its  entirety  and  all  the  large  peripheral 
branches  were  absolutely  smooth.  In  the  brain,  however, 
the  arteries  were  tortuous,  hard,  and  were  studded  with 
miliary  aneurysms.  It  is  not  possible  to  judge  accurately 
the  state  of  the  whole  arterial  system  by  the  stage  of  the 
lesion  in  any  one  artery ;  but  on  the  whole  one  may  say  that 
an  undue  thickening  of  the  radial  artery  indicates  analogous 
changes  in  the  mesenteric  arteries  and  in  the  aorta. 

So  far  as  the  anatomical  lesions  in  the  aorta  and 
branches  are  concerned,  there  is  much  uniformity  even 
though  the  etiologic  factors  have  been  diverse.  The  only 
difference  is  one  of  extent.  To  Thonia  we  owe  the  first 
careful  work  on  arteriosclerosis.  He  regarded  the  lesion 
in  arteriosclerosis  as  one  situated  primarih^  in  the  media; 
there  is  a  lack  of  resistance  in  this  coat.     His  views  are 


o4  Ar.TEPJO.SCLEnoSlS 

now  cliiefly  of  historical  interest.     As  the  author  under- 
stands him,  he  considered  a  rui)ture  in  the  media  to  be  the 
cause  of  a  local  widening  and  consequently  the  blood  could 
not  be  distributed  evenly  to  the  organ  which  was  supplied 
by  the  diseased  artery  or  arteries.     Moreover,  there  was 
danger  of  a  rupture  at  the  weak  spot  unless  this  were 
strengthened.    It  was  essential  for  the  even  distribution  of 
blood  that  the  lumen  be  restored  to  its  former  size.     Na- 
ture's method  of  repair  was  a  hypertrophy  of  the  subin- 
timal  connective  tissue  and  the  formation  of  a  nodule  at 
that  point.     The  thickening  was  compensatory,  resulting 
in  the  establishment  of  the  normal  caliber  of  the  vessel. 
Tlioma  showed  that  by  injecting  an  aorta  in  the  subject  of 
such  changes,  Avith  paraffin  at  a  pressure  of  160  mm.  of  mer- 
cury, these  projections  disappeared  and  the  muscle  bulged 
externally.     He  recognized  the  fact  that  the  character  of 
the  artery  changed  as  the  years  passed,  and  to  this  form 
he  gave  the  name,  primary  arteriosclerosis.    To  the  group 
of  cases  caused  by  various  poisonous  agents,  or  following 
high  peripheral  resistance  and  consequent  high  pressure, 
he  gave  the  name,  secondary  arteriosclerosis.     This  is  a 
useful  but  not  essential  division,  as  the  changes  which  age 
and  high  tension  produce  may  not  be  different  from  those 
produced  in  much  younger  persons  by  some  circulating 
poison.     And  most  important  to  bear  in  mind,  octogena- 
rians may  have  soft,  elastic  arteries. 

As  the  body  ages,  certain  cjianges  usually  take  place  in 
the  arteries  leading  to  thickening  and  inelasticity  of  their 
walls.  This  is  a  normal  change,  and  in  estimating  the  pal- 
pable thickening  of  an  artery,  such  as  the  radial,  the  age 
of  the  individual  nuist  always  be  considered. 

Thayer  and  Fabyan,  in  an  examination  of  the  radial 
artery  from  birth  to  old  age,  found  that,  in  general,  the 
artery  strengthens  itself,  as  more  strain  is  thrown  upon  it, 
by  new  elastica  in  the  intima  and  connective  tissue  in  the 
media  and  adventitia.    Up  to  the  third  decade  there  is  only 


PATHOLOGY  35 

a  strengtlioning  of  tlie  media  and  advcntitia.  During  the 
third  and  fourth  decades  there  is  also  distinct  connective 
tissue  thickening  in  the  intima.  "In  other  words,  the  strain 
has  begun  to  tell  upon  the  vessel  wall,  and  the  yielding  tube 
fortifies  itself  by  the  connective  tissue  thickening  of  the 
intima  and  to  a  lesser  extent  of  the  media."  By  the  fifth 
decade  the  connective  tissue  deposits  in  the  intima  are 
marked,  there  is  an  increase  of  fibrous  tissue  upon  the 
medial  side  of  the  intima  and,  in  lesser  degree,  throughout 
the  media.  ''Finally,  in  these  sclerotic  vessels  degenerative 
changes  set  in,  which  are  somewhat  different  from  those 
seen  in  the  larger  arteries,  consisting,  as  they  do,  of  local 
areas  of  coagulation  necrosis  with  calcification,  especially 
marked  in  the  deep  layers  of  the  connective  tissue  thicken- 
ings of  the  intima,  and  in  the  muscle  fibers  of  the  media, 
particularly  opposite  these  points.  These  changes  may 
.  .  .  go  on  to  actual  bone  formation."  The  mesenteric 
artery  differs  in  some  respects  from  the  radial,  but  in  the 
main,  the  changes  brought  about  by  age  are  the  same. 
Thayer  and  Fabyan  note  two  striking  points  of  difference: 
'*(!)  calcification  is  apparently  much  less  frequent  than  in 
the  radials;  (2)  in  several  cases  plaques  were  seen  with 
fatty  softening  of  the  deeper  layers  of  the  intima  and  super- 
ficial proliferation — a  picture  which  we  have  never  seen  in 
the  radial."     (See  Fig.  2.) 

Asehoff's  studies  of  the  aorta  show  tliat,  "in  infancy  the 
elastic  laminae  of  the  media  stand  out  sharply  defined,  well 
separated  from  each  other  by  the  muscle  layers,  which  are 
well  developed.  .  .  .  From  childhood  there  is  to  be  observed 
a  slowly  progressive  increase  in  the  elastic  elements  of  the 
media.  Xot  only  do  the  individual  lamella?  seen  in  cross- 
sections  become  thicker,  but  also  they  afford  an  increasing 
number  of  fine  secondary  filaments  feathering  off  from  these 
and  crossing  the  muscle  layer,  so  that  now  they  are  no 
longer  sharply  defined,  but  more  ragged  upon  cross-section. 
This  progressive  increase  attains  its  maximum  at  or  about 


IG 


ARTERIOSCLEROSIS 


the  age  of  thirty-five,  and  from  now  on  for  the  next  fifteen 
years  the  condition  is  relatively  stationary.  After  fifty 
there  is  to  be  observed  a  slowly  progressive  atrophy  of 
the  elastica.  Tlie  media  becomes  obviously  thinner  and 
presumably  weaker."  (Adami.)  It  has  also  been  found 
(Klotz)  that  after  the  age  of  thirty-five,  the  muscle  of  the 
media  begins  to  exhibit  fatty  degeneration  which  after  fifty 


Fig.  2. — Cross-section  of  a  coronary  arter}%  x50,  showing  nodnlar  sclerosis.  Xote  tlic 
heaping  u\>  of  cells  in  the  intima,  the  fracture  of  the  elastica,  and  the  destruction  of  the 
media  beneath  the  nodule.  The  primary  lesion  evidently  was  in  the  media.  The  thick- 
ened intima  is  the  effort  on  the  ]iart  of  nature  to  heal  the  breach.  At  such  places  as 
shown   hero   aneurysms   may    form.      (Microphotogra[)h.) 

years  is  well  marked.  The  fatty  degeneration  may  then 
give  place  to  a  calcareous  infiltration  or  the  fil)ers  may  un- 
dergo complete  absorption.  It  would  appear  that  the  thin- 
ning of  the  aortic  media  is  due  not  so  much  to  the  atrophy 
of  the  elastic  tissue  as  to  that  of  the  muscle  tissue.  The 
elastic  tissue  does  lose  its  specific  property  and  the  artery 
thus  becomes  practically  a  connective  tissue  tube. 


PATHOLOGY  37 

Sclieol  lias  made  very  careful  nieasurements  of  the 
ascending,  the  thoracic,  and  the  abdominal  aorta,  and  the 
pulmonary  artery.  He  found  that  from  birth  to  sixty 
years,  the  aorta  became  progressively  wider  and  lost  its 
elasticity.  The  pulmonary  changed  little,  if  at  all,  after 
thirty  to  forty  years,  and  where  before  it  was  wider  than 
the  aorta,  it  now  was  found  to  be  smaller.  In  chronic 
nephritis  both  were  widened.  The  continuous  increase  of 
width  and  length  of  the  aorta  stands  in  reverse  relationship 
to  the  elasticity  of  its  walls. 

Although  the  division  of  the  lesions  into  nodular,  diffuse, 
and  senile  has  been  the  usual  one,  it  is  better  to  separate 
three  groups  into  (1)  nodular,  (2)  diffuse  or  senile,  and  (3) 
syphilitic.  There  is  more  knoAvn  about  the  histology  of 
the  syphilitic  form  and  the  lesions  which  consist  of  pucker- 
ings  and  scars  seen  on  opening  an  aorta  just  above  the 
valves,  and  on  the  ascending  portion  of  the  arch  are  charac- 
teristic. A  macroscopic  examination  suffices  in  most  cases 
for  a  definite  diagnosis. 

In  the  nodular  form  the  lesions  are  found  on  the  aorta 
and  large  l)ranches  particularly  at  or  near  the  orifices  of 
branching  vessels.  These  nodules  may  increase  in  size, 
forming  rather  large,  slightly  raised  plaques  of  yellowish- 
white  color.  They  are,  as  a  rule,  irregularly  scattered 
throughout  the  aorta  and  branches  and  tend  to  be  more 
numerous  and  larger  in  the  abdominal  aorta.  The  initial 
lesion  is  in  the  media,  consisting  of  an  actual  dissolution  of 
this  coat  with  rupture  of  the  elastic  fibers  and  infiltration 
with  small  round  cells.  There  is  thus  a  weak  spot  in  the 
artery.  Hypertrophy  of  the  intimal  cells  takes  place, 
layer  upon  layer  being  added  in  an  attempt  to  strengthen 
the  vessel  at  the  injured  place.  Coincidently  with  this, 
there  is  thickening  by  a  connective  tissue  growth  in  the 
adventitia.  The  process  begins,  at  least  in  syphilis,  around 
the  terminals  of  the  vasa  vasorum.  It  will  be  recalled  that 
the  blood  supply  of  the  inner  portion  of  the  media  comes 


38  AllTElllO.SCLERO.SlS 

from  within  the  vessel  itself.  As  the  iiitimal  growth  in- 
creases, the  blood  supply  is  cut  off.  The  inevitable  result 
is  softening  of  the  portion  farthest  from  the  lumen  of  the 
vessel.  As  a  rule  there  has  been  a  sufficient  growth  of  con- 
nective tissue  in  the  media  and  adventitia  to  repair  the 
damage  done  to  the  media.  This  softening  and  dissolution 
gives  rise  to  a  granular  debris  composed  of  degenerated 
cells  and  fat.  This  is  the  so-called  atheromatous  abscess. 
There  are  no  leucocytes  as  in  ordinary  pus.  These  ''ab- 
scesses" are  frequent  and  in  rupturing  leave  open  ulcers 
with  smooth  bases,  the  atheromatous  ulcer.  A  further 
change  which  often  takes  place  is  calcification  of  the  bases 
of  the  ulcers  and  calcification  of  the  softened  spots  before 
rupture  takes  place.  This  only  occurs  in  advanced  cases. 
(See  Fig.  3.) 

Rather  contrary  to  what  one  w^ould  expect,  there  are  no 
new  cajjillaries  advancing  from  the  media  to  the  intima  in 
the  nodular  form  of  arteriosclerosis,  consequently  there  is 
no  granulation  tissue  to  heal  and  leave  scars.  It  must  be 
borne  in  mind  that  these  changes  rarely,  if  ever,  are  the 
only  ones  found  throughout  the  arterial  system.  Never- 
theless, the  manifold  changes,  as  will  be  shown  w^ithin,  ap- 
pear to  be  but  stages  of  one  primary  process. 

The  character  of  the  changes  which  are  known  as  diffuse 
arteriosclerosis  seems  to  have,  at  first  sight,  little  in  com- 
mon with  those  of  the  nodular  sclerosis.  The  aorta  may 
or  may  not  have  plaques  of  nodular  sclerosis,  while  the 
arteries,  such  as  the  radial  or  temporal,  may  be  beaded  or 
pipe  stem  in  hardness.  In  spite  of  these  far  advanced 
peripheral  lesions  the  aorta  may  appear  smooth  l)ut  it  is 
markedly  dilated,  particularly  the  thoracic  portion,  it  is 
noticeably  thinned  even  on  macroscopic  examination,  it 
has  elongated  as  evidenced  by  its  slight  tortuosity,  and  it 
has  lost  the  greater  part  of  its  elasticity.  The  abdominal 
aorta  is  not  so  extensively  affected,  although  this,  too,  shows 
some  elongation  and  slight  thinning.    This  is  considered  by 


PATHOLOGY 


39 


some  pathologists  to  be  tlie  uncomplicated  form  of  the  so- 
called  senile  arteriosclerosis.    It  is  more  of  the  nature  of  a 


Fig.  3. — Arteriosclerosis  of  the  thoracic  aiu!  abdominal  aorta,  showing  irregular 
nodules,  atheromatous  placiues,  denudation  of  the  intinia.  thin  plates  of  hone  scattered 
throughout  with  spicules  extending  into  the  lumen  of  the  vessel.  Note  the  contraction 
of  the  openings  of  the  large  branches,  the  rough  appearance  of  the  aorta  and  the  greater 
degree  of  sclerosis  of  the  upper  two-thirds,  i.  c.  of  the  aorta  above  the  diaphragm. 
This   aorta   in    the    recent   state   was   much    thickened   and   almost    inelastic. 

degenerative  change,  it  is  true,  but,  as  will  be  shown  later, 
it  has  its  beginnings,  at  times,  in  comparatively  young  per- 


40 


ARTEPtlOSCLEROSTS 


sons  and  its  cti()l()<;y  is  not  simple.  This  type  has  been 
studied  most  carefully  l)y  ]\loenckel)erg,  who  showed  that  on 
the  large  branches  of  the  aorta  there  were  depressions  due 


Fi^.  4. — Arteriosclerosis  of  the  arch  of  the  aorta.  Numerous  calcified  plaques, 
thickening  and  curling  of  the  aortic  valves,  giving  rise  to  insufficiency  of  the  aortic 
valves.      The    aortic    ring   is    rigid   and    not    much   dilated.      (Milwaukee    County   Hospital.) 

to  a  degeneration  of  the  middle  coat.     These  depressions 
encircled  the  vessel  to  a  greater  or  lesser  extent,  causing 


PATHOLOGY  41 

small  bulgiiigs  at  such  places  and  giving  to  the  vessel  a 
beaded  appearance.  On  viewing  such  an  artery  held  to  the 
light,  the  sacculated  spots  are  seen  to  be  much  thinner  than 
the    contiguous    normal    artery.      Associated    with    such 


Fig.  5. — Normal  aorta.  Compare  with  Fig.  3.  Note  the  perfectly  smooth,  glossy  ap- 
pearance of  the  intima.  The  openings  of  ell  the  intercostal  arteries  are  distinctly  seen. 
In  the  recent  state  this  artery  was  highly  elastic,  capable  of  much  stretching  both 
transversely   and   longitudinally. 

changes  in  the  aorta  and  large  branches  is  marked  sclerosis 
of  the  smaller  arteries.  Intimal  fibrosis  is  common,  together 
with  hypertrophy  and  fibrosis  of  the  middle  coat.  Not  in- 
frequently periarterial  thickening  is  also  seen.    Calcification 


42 


ARTERIOSCLEROSIS 


Fig.    6. — Radiogram    of   a  man   aged   seventy-five,    showing   calcification   of   both    radial    and 

ulnar   arteries. 


PATflOLOGY  4d 

of  the  media  is  found  and  is  said  to  be  preceded  by  liyper- 
tropliy  of  the  middle  coat. 

Pure  cases  of  this,  the  so-called  Moenckeberg  type,  are 
seen  but  seldom.  ]\rost  connnonly  there  are  nodules  and 
plaques  in  tlio  aorta  and  lai'<i'e  l)ranches  to.ii;ether  with  thin- 
ning and  sacculation  of  other  portions  of  the  vessels'  walls. 
While  the  two  processes  appear  at  a  glance  to  be  so  differ- 
ent from  each  other,  it  is  possible  for  them  to  have  a 
common  origin.  The  initial  lesion  is  in  the  media  but  the 
resulting  sclerotic  changes  depend  upon  the  kind  of  vessel, 
the  strength  of  the  coats,  the  pressure  in  the  vessel,  and 
other  causes. 

Thus  the  sclerosis  of  the  radials  of  such  an  extent  that 
these  arteries  are  easily  i^aljDable,  appears  to  be  a  different 
process  from  that  of  the  sclerosis  in  the  aorta,  yet  funda- 
mentally it  is  the  same.  The  difference  lies  in  the  ana- 
tomic structure  of  the  two  vessels,  and  possibly  also  in  the 
degree  of  stretching  and  strain  to  which  tlie  vessels  are 
subjected  at  every  heart  beat.  In  the  radial  artery  the 
media  as  usual  is  affected  first.  The  nmscle  cells  undergo 
degeneration  and  either  marked  thickening  takes  place  or 
sacculation  results,  depending  upon  the  severity  of  the  ex- 
citing cause.  Calcification  of  the  media  is  connnon.  This 
occasionally  takes  the  form  of  rings  encircling  the  vessel, 
and  gives  to  the  examining  finger  the  sensation  of  feeling 
a  string  of  fine  beads.  There  may  be  calcification  of  the 
sul)intimal  tissue  without  deposits  of  lime  salts  in  the  me- 
dia, but  this  is  more  connnonly  found  in  the  larger  artei-ies. 
When  the  calcification  occurs  in  plates  through  the  media, 
the  well  knoMm  pipe  stem  vessel  is  produced.     (Fig.  6.) 

The  senile  sclerosis  found  in  old  people  is  usually  a  com- 
bination of  the  ^loenckeberg  type  in  the  large  and  medium- 
sized  arteries,  and  the  nodular  type  in  the  aorta,  leading 
eventually  to  calcareous  intimal  deposits,  and  widened, 
elongated,  inelastic  aorta. 


44 


ARTERIOSCLEROSIS 

Syphilitic  Aortitis 


Tlie  scat  of  election  of  tlie  sypliilitic  poison  is  in  the  aorta 
jnst  al)ove  the  aortic  valves,  Fig-.  7,  and  in  the  ascending 


Fig.  7. — Syphilitic  aortitis  of  long  standing.  The  aortic  valves  are  curled  and 
thickened,  the  heart  is  enlarged  and  the  cavity  of  the  left  ventricle  is  dilated.  (Mil- 
waukee   County   Hospital.) 

portion  of  the  arch.    There  are  semitranslncent,  hyaline-like 
plaques  which  have  a  tendency  to  form  into  groups  and, 


PATHOLOGY  45 

instead  of  inidergoiiig  an  atheromatons  cliange  as  in  tlie  or- 
dinary nodular  form  of  arteriosclerosis,  they  are  prone  to 
scar  formation  witli  puckering,  so  that  macroscopically  the 
nature  of  the  process  may,  as  a  rule,  be  readily  diagnosed. 
Microscopically  the  process  is  found  to  be  a  subacute  in- 
flammation of  the  media,  which  has  been  called  a  mesaorti- 
tis.  There  is  marked  small  celled  infiltration  around  some 
of  the  branches  of  the  vasa  vasorum  and  there  appears  to  be 
actual  absorption  of  the  tissue  elements  of  the  middle  coat. 
This  is  accompanied  by  hypertrophy  of  the  intimal  tissue. 
There  follows  degeneration  in  the  deeper  portions  of  this 
new  tissue  and  new  cai)illaries  are  formed  which  have  tlieir 
origin  in  the  inflannnatory  area  in  the  media.  As  is  every- 
wliere  the  case  throughout  the  body,  granulation  tissue  in 
the  process  of  healing  contracts  and  forms  scars.  This  ex- 
plains the  scar  formation  in  the  aorta.  AVhen  the  process 
is  more  acute,  instead  of  there  being  a  reparative  attempt 
on  the  part  of  the  intima,  there  is  actual  stretching  of  the 
wall  at  the  weakened  spot  and  there  results  an  aneurysmal 
dilatation.  Spirochetae  pallidas  have  been  found  in  the  de- 
generated media  and  in  small  gummata  which  were  situated 
beneath  the  intima.  AVithin  the  past  years  it  has  been 
found  that  a  large  percentage  of  patients  with  cardiovascu- 
lar disease  give  the  AVassermann  reaction.  In  cases  of 
aortic  insuflfieiency,  the  reaction  is  present  in  almost  every 
case.  This  is  in  marked  contrast  to  the  cases  of  dilTuse  en- 
docarditis where  the  reaction  is  rarely  present. 

According  to  Adami  the  effects  of  syphilis  upon  the  aorta 
are  the  following:  (1)  the  primary  disturbance  is  a  granu- 
lomatous, inflannnatory  degeneration  of  the  media;  (2)  this 
leads  to  a  local  giving  way  of  the  aorta;  (3)  if  this  be 
moderate  it  results  in  a  strain  hypertrophy  of  the  intima 
and  of  the  adventitia,  with  the  development  of  a  nodose  in- 
timal sclerosis;  (4)  if  it  be  extreme,  there  results,  on  the 
contrary,  an  overstrain  atrophy  of  the  intima  and  aneurysm 
formation;  (5)   the  intimal  nodosities  are  here  not  of  an 


46  ARTERIOSCLEROSIS 

inflaniniatory  type  and  are  nonvascular,  altlioiigli,  with  tlie 
13rogressive  laying  down  of  layer  upon  layer  of  connective 
tissue  on  the  more  intinial  aspect  of  the  intima,  the  earlier 
and  deeper-placed  layers  of  new  tissue  gain  less  and  less 
nourishment,  and  so  are  lial)le  to  exhibit  fatty  degeneration 
and  necrosis;  (6)  these  products  of  necrosis  exert  a  chemo- 
tactic  influence  upon  the  nearby  vessels  of  the  medial  gran- 
ulation tissue,  with,  as  a  result,  (a)  a  secondary  and  late 
entrance  of  new  vessels  into  the  early  and  deeply-placed 
atheromatous  area,  (1))  a])sorption  of  the  necrotic  products, 
(c)  replacement  by  granulation  tissue,  (d)  contraction  of 
the  granulation  tissue,  and  (e)  depression  and  scarring  of 
the  sclerotic  nodules  so  characteristic  of  syphilitic  sclerosis. 
In  the  smaller  arteries  and  arterioles  the  arteriosclerotic 
process  appears  on  superficial  examination  to  be  a  different 
process  from  that  in  the  aorta  and  large  arteries,  but  the 
ditference  is  only  apparent.  It  will  be  recalled  that  there 
is  relatively  much  more  muscle  tissue  in  the  arterioles  than 
in  the  large  arteries.  The  size,  of  course,  is  much  less. 
Large  nodular  plaques  are  not  possible.  Tiie  atheromatous 
degeneration  is  not  marked.  In  the  smaller  muscular 
arteries  is  seen  the  intimal  proliferation,  the  stretching  of 
the  Moenckeberg  type,  and  the  calcification  of  the  media 
rather  than  the  intima.  The  media  is  thinned  beneath  the 
marked  intimal  proliferation  so  that  the  artery  exhibits 
translucent  areas  when  lield  to  the  light.  Again,  there  is 
seen  degeneration  of  the  muscle  and  replacement  by  con- 
nective tissue  with  or  without  hypertrophy  of  the  intima. 
In  the  arterioles  three  kinds  of  changes  occur:  a  muscular 
hypertrophy;  a  fibrosis  of  all  the  coats;  or  a  marked  prolif- 
eration of  the  intimal  endothelium.  The  last  two  are 
jjrobably  the  same  jjrocess,  the  connective  tissue  having  its 
origin  in  the  proliferated  endothelial  cells.  Such  a  deposi- 
tion of  layer  upon  layer  of  cells  in  an  arteriole  and  the  re- 
sulting fibrosis  leads  to  the  condition  of  disappearance  of 
the  lumen  of  the  vessel,  endarteritis  obliterans.     This  ob- 


PATHOLOGY  47 

literating  endarteritis  is  not,  of  course,  due  alone  to 
sypliilis.  Syphilis  is  onh^  a  type  of  poison  wliieli  produces 
sucli  changes  as  have  been  described  above.  It  is  in  the 
organs  such  as  the  kidney,  liver,  spleen,  and  intestines  that 
one  sees  the  most  perfect  examples  of  this  obliterating 
endarteritis.  Endarteritis  deformans  is  a  term  applied  to 
the  condition  of  the  arteries  as  a  result  of  irregular  thick- 
enings and  deposits  of  lime  salts  in  the  walls.  These 
changes  give  rise  to  marked  tortuosity  of  the  vessels. 

Occasionally  such  an  obliterating  process  takes  place  in 
a  larger  artery.  A  thrombus  forms  and  by  a  process  of 
central  softening,  new  channels  permeate  the  thrombus, 
thus  restoring  to  some  extent  the  function  of  the  vessel. 

That  the  same  process  leads  at  one  time  to  thinning  and 
at  another  time  to  thickening  of  the  arterial  walls  has  been 
noted  above.  Prof.  Adami  holds  that  the  regular  develop- 
ment of  layer  upon  layer  of  new  connective  tissue  is  non- 
inflammatory. He  calls  it  a  "strain  hypertrophy."  It  is 
analogous  to  the  localized  hyi^ertrophy  of  bone  where  the 
muscle  tendons  are  attached,  as  is  so  frequently  seen  in 
athletes.  The  increased  tension  on  connective  tissue,  pro- 
vided that  it  is  not  overstrained,  leads  to  its  overgrowth, 
but  only  when  there  is  sufficient  nourishment.  Such  con- 
ditions are  adequately  fulfilled  in  the  arteries.  When  a 
local  giving  way  under  pressure  occurs  in  the  media,  the 
intima  is  put  on  the  stretch  (see  Fig.  8),  and  there  results 
a  hypertrophy  of  the  intima  until  the  volume  of  the  new 
tissue  and  the  resistance  which  this  affords  to  the  mean  dis- 
tending force,  balances  the  loss  sustained  by  tlie  weakened 
media.  When  the  balance  is  struck,  the  hypertrojihy  is 
arrested.  The  youngest  tissue  is  thus  found  directly  be- 
neath the  endothelium.  Xow  should  this  local  weakening  of 
the  media  have  an  acute  origin,  instead  of  a  stimulus  to 
growth  there  is  overstrain,  and  there  is,  in  consequence,  not 
hypertrophy  Init  atrophy.  The  beginning  process  is  liere 
a  mesaortitis,  but  the  acuteness  of  tlie  poison,  and  the  pres- 


48 


ARTERIOSCLEROSIS 


sure  from  witliin  tlie  artery  so  stretches  the  artery  that 
tliere  is  no  compensatory  hypertrophy,  hut  a  tliinning,  and 
the  ground  is  prejoared  for  aneurysmal  dilatation  or  pouch- 
ing. 

Again,  one  not  infrequently  encounters  intimal  nodosities 
when  the  underlying  media  appears  of  normal  thickness. 
The  explanation  of  this  apparent  exception  is  that  the  me- 
dia in  the  living  aorta  is  actually  thinned,  but  the  layers  of 
subintimal  tissue  deposited  over  the  weak  spot  due  to  strain 
hypertrophy  become  bulged  inward  when  the  pressure  is 


Fig.  8. — I,  media  weakened  at  M'  with  overgrowth  of  intima  filling  in  the  depression. 
II,  with  postmortem  rigor  and  contraction  of  the  muscles  of  the  media  and  removal 
of  the  blood  pressure  from  within,  the  stretched  media  at  M''  contracts;  the  intimal 
thickening  thus  projects   into  the  arterial   lumen.      (After  Adami.) 

relieved,  as  at  postmortem.  The  media  has  not  lost  all  of 
its  elasticity  (see  Fig.  9),  hence  it  contracts  and  there  is 
the  appearance  of  a  nodule  on  the  intima  l)eneath  which  is  a 
media  equal  in  thickness  to  that  of  the  healthy  surrounding 
media. 

The  essential  lesion  in  arteriosclerosis  of  the  aorta  and 
large  arteries  is  a  degeneration  in  the  middle  coat.  This 
may  be  brought  about  by  a  variety  of  poisons  circulating  in 
the  body.    In  syphilis,  for  example,  the  initial  lesion  has 


PATHOLOGY 


49 


been  sliown  to  be  a  mesaortitis.  Tlie  media  seems  to  be  dis- 
solve<t,  tlie  artery  is  consequently  thinned,  tliere  is  actual 
depression  along  tlie  level  of  the  vessel.  The  elastic  fibers 
disappear  and  small-celled  infiltration  takes  its  i)lace.    The 


Jnt- 


\~  Med. 


Fig.  9. — Schematic  representation  of  the  increased  strain  brought  to  hear  upon  the 
cells  of  the,  intirna,  Int.,  when  the  media,  Med.,  undergoes  a  localized  expansion  through 
relative    weakness.      (After   Adanii.) 


intima  hypertrophies,  layer  upon  layer  being  added  in  an 
attempt  to  restore  the  strength  of  the  vessel.  There  is  also, 
as  a  rule,  rather  pronounced  hyijertroi^hy  of  the  adventitia. 


50  A1{TER  I OSCLEROSIS 

Experimental  Arteriosclerosis 

Within  tlie  past  fe^^'  yeai's  many  workers  liave  attempt(Ml 
by  various  means,  to  produce  arterial  lesions  in  animals, 
cliiefly  raljl)its  and  dogs.  ''I'lie  present  status  is  somewhat 
chaotic,  some  affirming  and  some  denying  that  arterial 
changes  follow  the  varions  methods  employed.  Following 
the  injection  of  small,  repeated  doses  of  adrenalin  over  a 
certain  period  of  time,  changes  occur  in  the  arteries  of 
rabbits  which  are  arteriosclerotic  in  type,  the  essential 
lesion  being  a  degeneration  of  the  muscular  and  elastic  tis- 
sue of  the  media  with  the  consequent  production  of  aneu- 
rysm in  the  vessel.  This  is  said  by  some  to  be  ciuite  like 
the  type  of  arteriosclerosis  in  man  which  has  been  so  Avell 
described  by  Moenckeberg.  The  degenerations  in  the  ar- 
teries following  the  experimental  lesions  are  of  the  nature 
of  a  fatty  metamorphosis,  and  later  proceed  to  calcification. 
Barium  cldoride,  digitalin,  j^hysostigmin,  nicotin  and  other 
substances,  as  well  as  adrenalin,  have  been  found  to  exert 
a  selective  toxic  action  on  the  nuiscle  cells  of  the  middle 
coat  of  the  aorta.  The  infundibular  portion  of  the  pituitary 
body,  the  portion  which  is  developed  from  the  infundibulum 
of  the  brain,  possesses  an  internal  secretion,  which,  injected 
intravenously,  causes  a  marked  rise  of  blood  pressure  and 
slowing  of  the  heart  beat.  So  far  as  I  know,  this  active 
principle  of  the  gland  has  not  been  used  in  an  attempt  to 
produce  experimentally  the  lesions  of  arteriosclerosis. 

AVacker  and  Hueck  succeeded  in  producing  aortic  dis- 
ease in  rabbits  which  they  considered  to  be  in  many  points 
quite  like  human  arteriosclerosis.  They  injected  the  rab- 
bits intravenously  with  cholesterin.  They  feel  that  this  is 
of  great  importance  in  view  of  the  fact  that  exercise  (mus- 
cle metabolism)  dyspnea,  certain  poisons,  as  well  as  adren- 
alin, and  even  adrenal  extirpation  occasion  a  high  choles- 
terin content  of  tlie  blood.  Anitschow's  experiments  are 
confirmatory.    He  fed  rabbits  on  large  amounts  of  clioles- 


PATHOLOGY  51 

terin-coiitainiiig  substances  (yolk  of  egg,  brain  tissue)  and 
pure  cliolesterin  and  found  changes  in  tiie  intima  and  inner 
portion  of  tlie  media  consisting  of  fatty  infiltration  between 
the  muscle  and  elastic  fibres,  advent  of  small  round  cells 
and  large  phagocytic  cells  containing  fat  droplets  of  clioles- 
terin esters.  The  elastic  fibres  were  dissolved,  broken  up 
into  fibrilltX)  and  these  seemed  to  be  al)Sorbed.  The  internal 
elastic  lamina  as  such  disa^jpeared  and  the  inner  layer  of 
the  aorta  fused  with  the  middle  coat.  He  considers  these 
changes  to  be  quite  analogous  to  those  found  in  human 
aortas. 

Oswald  Loeb  produced  changes  in  the  arteries  of  rabbits 
by  feeding  them  sodium  lactate  (lactic  acid).  His  controls 
fed  on  other  acids  became  cachectic,  but  showed  no  arterial 
changes.  He  further  found  that  in  100  gni.  of  human  Ijlood 
there  was  normally  from  15  to  30  mg.  of  lactic  acid.  After 
lieayy  work,  he  found  as  much  as  150  gm.  He  considers 
that  after  adrenalin  or  nicotin  injections,  the  function  of  the 
liver  is  so  disturbed  that  lactic  acid  is  not  bound.  The  ar- 
teriosclerosis is  actually  due  to  the  presence  of  free  lactic 
acid  in  the  circulation.  He  succeeded,  also,  in  jDroducing 
lesions  of  the  intima  in  a  dog  fed  for  a  long  time  on  pro- 
tein poor  diet,  plus  lactic  acid  and  sodium  lactate. 

Another  investigator,  Steinbiss,  fed  rab))its  on  animal 
proteins  only,  a  diet  totally  foreign  to  their  natural  habits. 
He  succeeded,  however,  in  keex)ing  some  alive  for  three 
months.  He  also  tried  various  sul)stances  and  in  the  general 
conclusions  says  that  no  aortic  changes  could  be  produced 
in  animals  kei)t  in  jiatural  living  conditions  by  any  mechan- 
ical means,  increase  of  blood  pressure,  digital  compression, 
hanging  by  hind  legs,  etc.  In  infectious  diseases,  especially 
septic,  widespread  sclerotic  changes  occurred  in  the  aorta. 
A  most  suggestive  conclusion  in  this  "the  most  imiwrtant 
result  of  feeding  rabbits  with  animal  proteins  is,  along  with 
a  constant  glycosuria,  disease  of  the  aorta  and  peripheral 
arteries  which  is  identical  with  changes  in  the  aorta  2>i'o- 


52  ARTERTOSCLEROSIS 

diieed  by  injections  of  adrenalin.  Tlie  degree  of  disease  of 
the  circulatory  system  increases  witli  the  duration  of  the 
experiment." 

By  a  small  addition  of  vegetable  to  the  protein  diet,  the 
lives  of  the  animals  were  prolonged  at  will.  AVitli  this 
moditication  of  the  experiment,  the  findings  in  the  vessel 
walls  were  noticeably  altered.  The  changes  affected  chiefly 
the  intima,  to  less  degree  the  media,  and  histologically  were 
very  much  like  human  intimal  disease. 

I  have  been  unable  to  produce  the  slightest  arterial  le- 
sions in  rabbits  l)y  intravenous  injections  of  lead.  Froth- 
ingham  had  no  success  feeding  animals  with  lead.  In  a 
study  of  autopsy  material  from  i:)ersons  up  to  40  years,  who 
died  of  infectious  disease,  he  found  changes  in  the  arteries 
of  those  who  had  succumbed  to  infection  with  the  pus  cocci 
or  to  very  severe  infectious  disease.  These  changes  were, 
however,  localized,  and  were  not  like  those  of  the  general 
diffuse  arteriosclerosis. 

Adler  has  recently  reported  experiments  on  dogs,  to 
which  he  fed  or  injected  intravenously  various  substances 
supjoosed  to  induce  arteriosclerotic  changes,  lie  was  una- 
ble to  find  any  arterial  lesions  comparable  to  human  arterio- 
sclerosis. 

The  difficulty  experienced  by  experimenters  is  not  sur- 
prising when  the  character  of  the  changes  is  considered. 
Arteriosclerosis  is  not  an  acute  process.  In  its  very  nature, 
it  is  of  months'  or  years'  standing,  the  specific  changes  are 
of  slow  growth,  and  more  in  the  nature  of  degeneration.  It 
would  seem  that  a  very  careful  study  of  the  histories  of 
those  with  arteriosclerosis  and  a  final  examination  upon  the 
actual  tissue  might  eventually  give  us  data  for  the  etiology. 

The  most  frequent  site  of  disease  in  these  experimental 
lesions  is  the  thoracic  aorta,  and  it  is  there  also  that  t^je 
most  severe  changes  are  seen.  While  the  toxic  action  is  felt 
in  the  vessels  all  over  the  l)ody,  the  lesions  are,  as  a  rule, 
scattered  and  small.     The  thoracic  aorta  stands  the  brunt 


PATHOLOGY  5d 

of  tlie  liigli  in-eyyure,  and  tliis  eombined  with  tlio  i)oisoiioiis 
action  of  the  drug  or  drugs,  results  in  the  formation  of  a 
fusiform  aneurysmal  dilatation  which  stops  at  the  dia- 
phragmatic opening.  The  aortic  oj)ening  in  the  diaphragm 
seems  to  act  as  a  flood  gate,  allowing  only  a  certain  amount 
of  blood  to  flow  through,  and  thus  the  abdominal  aorta  is 
protected  to  a  great  extent  from  the  deleterious  effects  of 
increased  i^ressure.  Focal  degenerative  lesions  are,  how- 
ever, found  in  the  abdominal  a^'Tta. 

Changes  somewhat  analogous  Iw  those  found  in  the  human 
aorta  as  the  result  of  intimal  jDroliferations,  are  produced 
in  animals  by  the  toxins  of  the  typhoid  bacillus  and  the 
Strei)tococcus  pyogenes.  Clinically,  Thayer  and  Brush 
have  found  that  the  arteries  of  those  who  have  recovered 
from  an  attack  of  typhoid  fever  are  more  palpable  than  the 
arteries  of  average  individuals  of  equal  age  who  have  never 
had  the  disease. 

Experimentally,  the  changes  caused  by  the  toxins  above 
noted  are  proliferations  of  cells  in  the  intinia  and  subintimal 
tissues,  and  a  breaking  up  of  the  internal  elastic  laminae 
into  several  parallel  layers  which  stretch  themselves  among 
the  proliferating  cells.  The  diphtheria  toxin,  on  the  con- 
trary, produces  a  lesion  more  like  that  caused  by  adrenalin. 
All  pathologists  are  not  agreed  as  to  whether  the  experi- 
mental lesions  produced  by  blood  pressure  raising  drugs 
are  similar  to  the  arteriosclerotic  changes  in  the  arteries 
of  man. 

Sojue  of  the  work  on  rabbits  has  been  discredited  for  the 
reason  that  arteriosclerosis  appears  si)ontaneously  in  about 
fifteen  jier  cent  of  all  la])oratory  rab])its.  Furthermore, 
comparatively  young  rab])its  liave  been  found  with  arterio- 
sclerosis. 0.  Loeb,  however,  denies  this.  lie  has  examined 
in  the  course  of  eight  years  483  healthy  ral)bits  and  never 
found  arterial  changes.  The  spontaneous  lesions  can  not 
be  distinguished  histologically  from  those  due  to  adrenalin. 


54  ARTERIOSCLEROSIS 

They  differ  inaeros('oi)ieally  in  that  tlie  lesion  is  usually 
limited  to  a  few  foci  near  the  origin  of  the  aorta. 

Lesions  produced  hy  the  drugs  enumerated  al)ove  repre- 
sent one  type  of  exi^erimental  arteriosclerosis.  More  in- 
teresting and  important  are  the  experiments  which  seem  to 
show  that  liigli  tension  alone  is  capal)le  of  producing  lesions 
in  arteries  whicli  in  all  respects  correspond  to  Adami's 
strain  hypertrophy  and  overstrain  theory.  It  has  ])een 
shown  that  when  a  portion  of  vein  is  placed  under  condi- 
tions of  high  arterial  pressure,  as  in  a  transplantation  of  a 
portion  of  vein  into  a  carotid  artery,  the  vein  imdergoes 
marked  connective  tissue  hypertrophy  which  includes  all 
the  coats.  This  is  evidently  strain  hyj)ertroi)hy.  Again,  it 
has  been  demonstrated  that  hy  suspending  a  previously 
healthy  rabbit  by  the  hind  legs  for  three  minutes  daily  over 
a  period  of  three  to  four  months,  there  resnlts  hyi^ertrophy 
of  the  heart  with  tliinning  and  dilatation  of  the  arch  and  the 
upper  part  of  the  thoracic  aorta.  Xo  change  was  found  in 
the  abdominal  aorta.  The  carotids,  however,  were  larger 
than  nonnal  and  they  showed  typical  intimal  sclerosis  with 
connective  tissue  thickening. 

Neither  I  nor  others  have  been  able  to  confirm  this  ex- 
periment, so  it  is  very  doubtful  whether  mechanical  pres- 
sure alone  can  produce  true  arteriosclerosis.  Some  evi- 
dence is  adduced  to  bear  on  this  point,  however,  in  the  fact 
that  sclerosis  of  the  pulmonary  artery  follows  often  upon 
mitral  stenosis.  Yet  we  do  not  know  but  that  factors  other 
than  pressure  alone  produce  the  arteriosclerotic  change  in 
such  cases,  so  we  are  forced  back  on  our  conclusion  ex- 
pressed above;  viz.,  that  experiments  on  animals  fail  to 
sustain  the  purely  mechanical  origin  of  arteriosclerosis. 

The  changes  in  the  intinia  constitute  the  effort  on  the 
part  of  nature  to  repair  a  defect  in  the  vessel  wall  which  is 
to  compensate  for  the  weakened  media  and  the  widened 
lumen.     This  applies  only  to  true  arteriosclerosis,  not  to 


PATHOLOGY  00 

tlie  condition  |)roducod  experiniontally  by  tlie  toxin  of  tlie 
typhoid  bacillus,  for  example. 

AVlien  an  artery  loses  its  elasticity  and  begins  to  liave 
connective  tissue  deposited  in  its  walls,  the  pressure  of  the 
blood  stretches  the  vessel  which  is  now  no  longer  capable  of 
retracting  when  the  pulse  wave  has  passed,  and,  in  conse- 
quence, the  artery  is  actually  lengthened.  This  necessarily 
causes  a  tortuosity  of  the  vessel  which  can  be  easily  seen  in 
such  arteries  as  the  temporals,  l)rachials,  radials,  and  other 
arteries  near  the  surface  of  the  skin. 

The  exact  mechanism  of  increase  of  l)lood  pressure  is  not 
satisfactorily  explained.  The  smaller  arteries  all  over  the 
body  are  supplied  with  vasoconstrictor  and  vasodilator 
nerve  fibers  from  the  sympathetic  nervous  system.  Nor- 
mally when  an  organ  is  actively  functionating  the  vessels 
are  widely  dilated  and  the  flow  of  blood  is  rapid.  Among 
the  many  factors  which  influence  blood  pressure  and  blood 
supply  must  be  reckoned  the  psychic. 

AVe  know  that  normally  there  is  a  certain  resistance 
offered  to  the  propulsion  of  blood  through  the  arteries  by 
the  contraction  of  the  heart.  This  tonus  is  essential  to  the 
maintenance  of  an  equalized  circulation.  The  nniscular 
arterioles  throughout  the  body  by  their  tonus  serve  to  keep 
up  the  normal  blood  pressure  and  to  distribute  the  blood 
evenly  to  the  various  organs.  Contraction  of  a  large  area 
of  arterioles  increases  the  blood  pressui-e  and,  strangely 
enough,  the  arteries  respond  to  increased  arterial  pressure, 
not  by  dilatation,  but  l)y  contraction.  It  would  aj^pear  that 
rise  of  blood  pressure  tends  to  throw  increased  work  upon 
the  nmsculature  of  the  arterioles.  This  may  be  sufficient 
only  to  cause  them  to  hyj)ertroi)liy,  but  further  strain  may 
easily  lead  to  exhaustion  and  to  dilatation.  ''As  a  result 
strain  liypertrophy  of  the  intima  shows  itself  with  thicken- 
ing, and  it  may  also  be  of  the  adventitia,  resulting  in  chronic 
periarteritis.  And  now  with  continued  degeneration  of  the 
medial  muscle  in  those  nuiscular  arteries,  fibrosis  of  the 


56 


ARTERrOSCLEROSIS 


media  Jiuiy  also  sliow  itself.  I  would  tliiis  regard  muscular 
liypertropliy  of  the  arteries  and  fibrosis  of  tlie  different 
coats  as  dilferent  stages  in  one  and  the  same  process. 
AVlietlier  these  i)eripheral  changes  are  the  more  marked,  or 
the  central,  dej^ends  ni)on  the  relative  resisting  power  of 


Fig.  10. — Cross-section  of  a  small  artery  in  the  mesentery.  Note  that  the  vessel  ap- 
pears capable  of  being  much  vviflened.  The  internal  elastic  lamina  is  thrown  into  folds 
somewhat  resembling  the  convolutions  of  the  brain.  Note  also  that  the  middle  coat 
of  the  artery  is  composed  almost  entirely  of  muscle.  The  enormous  number  of  such 
vessels  in  the  mesentery  and  intestines  exjjlains  the  ability  of  the  splanchnic  area  to 
accommodate  the  greater  part  of  the  blood  in  the  body.  Universal  constriction  of  these 
vessels  would  naturally  render  the  intestines  anemic.  The  vasomotor  control  of  these 
vessels  plays  an  important  role  in  the  distribution  of  the  blood.  Small  arteries  in  the 
skin  and  in  other  organs,  possibly  the  brain,  have  a  similar  function.  (Microphotograph, 
highly  magnified.) 


the  elastic  and  nmscular  arteries  of  the  individual  respec- 
tively."    (Adami.) 

It  is  conceivable  that  in  one  section  of  the  body  the  vessels 


PATHOLOGY  57 

may  be  markedly  contracted,  but  if  tliere  is  dilatation  in 
some  other  part  tliere  will  be  no  increased  work  on  the  part 
of  the  heart,  and  theoretically,  there  should  be  no  rise  of 
blood  pressure.  The  vascular  system,  however,  while  lik- 
ened to  a  system  of  rubber  tubes,  must  be  regarded  as  a 
very  live  system,  every  subsystem  having  the  property  of 
separate  control. 

For  blood  tension  to  be  raised  all  over  the  body,  condi- 
tions must  favor  the  generalized  contraction  of  a  large  area 
of  arterioles.  Some  authors  consider  that  the  so-called 
viscosity  of  the  blood  also  is  a  factor  in  the  causation  of 
increased  tension.  The  usual  cause  for  the  high  tension  is 
probably  the  presence  in  the  blood  of  some  poisonous  sub- 
stance. 

It  is  held  by  some  authors  that  the  great  splanchnic  area 
is  capable  of  holding  all  the  blood  in  the  body  and  in  respect 
of  its  liabilit}^  to  arteriosclerosis,  it  is  second  only  to  the 
aorta  and  coronary  arteries.  The  enormous  area  of  the 
skin  vessels  could  probably  contain  most  of  the  blood. 
The  tone  of  the  vasoconstrictor  center  controls  the  distribu- 
tion of  blood  throughout  the  body.  The  fact  that  the  ves- 
sels in  the  splanchnic  area  are  frequently  attacked  by 
sclerotic  changes  means,  as  a  rule,  increase  of  work  for 
the  heart.*  The  resistance  offered  to  the  passage  of  the 
blood  must  be  great  and  signifies  that,  for  blood  to  travel  at 
the  same  rate  that  it  did  before  the  resistance  set  in,  more 
power  must  be  expended  in  its  proj^ulsion.  In  other  words, 
the  heart  nmst  gradually  become  accustomed  to  the  changed 
conditions,  and,  as  a  result  of  increased  work,  the  muscle 
hypertrophies.     (See  Fig.  11.) 

In  diffuse  arteriosclerosis  accompanied  by  chronic  nephri- 
tis the  heart  is  always  hypertrophied.    This  is  a  result,  not 


*Longcope  and  McClintock,  however,  conclude  that  permanent  constriction  of  the 
superior  mesenteric  artery  and  celiac  axis,  as  well  as  gradual  occlusion  of  one  or  both 
of  these  vessels,  may  be  present  in  dogs  for  at  least  live  months  without  giving  rise  to 
definite  and  constant  elevation  of  blood  pressure  or  to  hyjtertrophy  of  the  heart.  Further, 
they  have  been  unable  to  find  at  autopsy  on  man  a  definite  association  between  sclerosis 
of   the   abdominal   aorta   and   great   splanchnic   vessels   and   cardiac    hypertrophy. 


58 


ARTERIOSCLEROSIS 


a  cause  of  tlio  condition.  In  tlio  pure  type,  there  is  liyper- 
tropliy  only  of  the  h^ft  ventricle  without  dilatation  of  the 
chamber.  The  nuiscle  fil)ers  are  increased  in  number  and  in 
size,  and  there  are  frequently  areas  of  fibrous  myocarditis 
due  to  necrosis  caused  by  insufficient  nutrition  of  parts  of 
the  muscle.  In  these  cases  the  coronary  arteries  share  in 
the  generalized  arteriosclerotic  process.  The  openings  of 
the  arteries  behind  the  semilunar  valves  may  be  very  small. 


Fig.  11. — Enormous  hypertToi)hy  of  left  ventricle  probably  due  to  prolonged  in- 
creased peripheral  resistance.  Note  that  the  whole  anterior  surface  of  the  heart  is  occu- 
pied by  the  left  ventricle.  The  right  ventricle  does  not  appear  to  be  much  affected. 
x2/3. 


There  is  often  thickening  and  puckering  of  the  aortic  valves 
and  of  the  anterior  leaflet  of  the  mitral  valve  leading,  at 
times,  to  actual  insufficiency  of  the  orifice.  Later,  when  the 
heart  begins  to  weaken,  there  is  dilatation  of  the  chambers 
and  loud  murmurs  result,  caused  liy  the  inaliility  of  the  non- 
distensible  valves  to  close  the  dilated  orifices.  Until  the 
compensation  is  established,  it  is  impossible  to  say  whether 
or  not  true  insufficiency  is  present. 


PATTIOLOGY  59 

111  senile  arteriosclerosis  there  is  tlie  pliysiolo^'ic  atrophy 
of  the  media  to  be  reckoned  with.  This  change  has  already 
been  referred  to.  When  such  degeneration  has  taken  place, 
the  normal  blood  pressure  may  be  sufficient  to  cause  stretch- 
ing of  the  already  weakened  media  with  or  without  hyper- 
trophy of  the  intima.  The  arteries  may  be  so  lined  with 
deposits  of  calcareous  matter  that  they  appear  as  pipe 
stems.  More  frequently  there  are  rings  of  calcified  material 
placed  closely  together  or  irregular  beading,  giving  to  the 
palpating  finger  the  impression  of  feeling  a  string  of  very 
fine  beads.  The  arteries  are  often  tortuous,  hard,  and  are 
absolutely  nondistensil^le.  At  times  no  pulse  wave  can  be 
felt. 

The  larger  arteries  such  as  the  brachials  and  femorals 
are  most  affected.  The  walls  become  thinned  and  show 
cracks,  and  areas  apparently,  but  not  actually  denuded  of 
intima.  Yellowish-Avhite,  irregular,  raised  plaques  are  scat- 
tered here  and  there.  Interspersed  among  these  areas  are 
irregularly  shaped  clean-cut  ulcers  having  as  a  rule  a 
smooth  base,  and  frequently  on  the  base  is  a  thin  plate  of 
calcified  matter.  The  color  of  these  denuded  areas  is  usu- 
ally brownish  red  or  reddish  brown.  AVhite  thrombi  may 
be  deposited  on  these  areas.  The  danger  of  an  embolus 
plugging  one  of  the  smaller  arteries  is  great  and  probably 
happens  more  often  than  we  think.  The  collatei-al  circula- 
tion is  able  to  supjily  the  thrombosed  area.  Should  the 
thrombus  be  on  the  carotid  arteries,  hemiplegia  may  result 
from  cerebral  embolism.  On  microscopic  examination  of 
the  arteries  there  is  seen  extreme  degeneration  of  all  the 
coats,  the  degeiKU-ation  of  the  media  leading  almost  to  an 
obliteration  of  that  coat.  On  seeing  such  arteries  as  these 
one  wonders  how  the  circulation  could  have  been  main- 
tained and  the  organs  nourished.  Senile  atrophy  of  the 
internal  organs  naturally  goes  hand  in  hand  with  such 
arterial  changes. 

There  is,  as  a  rule,  no  increase  in  arterial  tension;  on  the 


GO  AIITERIOSCLEROSIS 

contrary,  the  pressure  is  apt  to  Ijc  low.  Tliis  is  readily 
iiiiderstood  Avlieii  the  heart  is  seen.  This  organ  is  small, 
the  nnisc'le  is  much  thinned,  it  is  flahhy  and  of  a  hrownisli 
tint,  the  so-called  ^'hrown  atrophy."  Microscopically, 
there  is  seen  to  l)e  nuich  fi'agmentation  of  the  fibers  with 
a  marked  increase  of  the  brown  pigment  granules  which 
surround  the  cell  nuclei.  Cases  are  seen,  however,  in  which 
blood  pressure  increases  as  the  jxitient  grows  older.  The 
hearts  in  sncli  cases  are  more  or  less  hypertrophied  and 
show  extensive  areas  of  fibroid  myocarditis. 

From  what  lias  been  said,  it  follows  that  hypertension 
alone  may  be  the  cause  of  arteriosclerosis;  that  certain 
poisons  in  the  blood  which  attack  the  media  and  cause  it 
to  degenerate  and  weaken  cause  arteriosclerosis  without 
increased  blood  i^ressure;  that  the  normal  blood  pressure 
may  be,  for  the  artery  which  is  j)hysiologically  weakened  in 
an  individual  over  fifty,  really  hypertension,  and  arterio- 
sclerosis may  result.  Our  observations  lead  us  to  believe 
that  the  process  is  at  bottom  one  and  the  same.  The  dif- 
ferent types  noted  clinically  depend  upon  the  nature  of  the 
etiologic  factors  and  the  kind  of  arterial  tissue  with  wliich 
the  individual  is  endowed.  This  view  at  least  brings  some 
order  out  of  previous  chaos,  and  corresponds  well  with  our 
present  knowledge  of  the  disease. 

There  are  many  cases  of  arteriosclerosis  which  lead  to 
definite  interference  with  the  closure  of  the  valves  of  the 
heart,  particularly  the  aortic  and  the  mitral.  It  has  been 
said  that  puckerings  of  the  valves  frerpiently  occur  (Fig. 
12).  This  arteriosclerotic  endocarditis  at  times  leads  to 
very  definite  heart  lesions,  chiefiy  aortic  or  mitral  insuffi- 
ciency, or  both  with,  at  times,  nmrnmrs  of  a  stenotic  char- 
acter at  the  l)ase.  There  is  rarely  true  aortic  stenosis, 
however.  Tlie  nmrnmr  is  caused  by  the  passage  of  the 
blood  over  the  roughened  valves  and  into  the  dilated  aorta. 
Aortic  stenosis  is  one  of  the  rarest  of  the  valvidar  lesions 
affecting  the  valves  of  the  left  heart,  and  should  be  diag- 


PATHOLOGY 


Gl 


nosed  only  when  all  factors,  including  the  typical  pulse 
tracings,  are  taken  into  consideration. 

The  kidneys,  as  a  rule,  show  extensive  sclerosis.  They 
are  small,  firm,  and  contracted  and  not  always  to  he  dif- 
ferentiated from  the  contracted  kidneys  of  chronic  inflam- 
mation. The  lesions  of  tlie  arteriosclerotic  kidney  are  due 
to  narrowin""  and  eventual  o])struction  of  the  afferent  ves- 


Fig.  12. — Aortic  incompetence  with  hypertro|)hy  and  dilatation  of  left  ventricle,  the 
result  of  arteriosclerosis  affecting  the  aortic  valves.  Note  how  the  valves  have  been  curled, 
thickened,  and  shortened,  the  edges  of  valves  heing  a  half  inch  below  the  upper  points 
of  attachment.  The  anterior  coronary  artery  is  shown,  the  lumen  narrowed.  (Reduced 
one-half.) 


sels.  The  organs  are  usually  Ijright  red  or  grayish  red  in 
color.  At  times  there  is  marked  fatty  degeneration  of 
cortex  and  medulla,  giving  to  them  a  yellowish  streaking. 
The  capsule  is  here  and  there  adherent,  the  cortex  is  much 
thinned  and  irregular.     The  surface  j^resents  a  roughly 


62  AllTICniOSCLEUOSLS 

fti-anu]ar  a])i)earaiK'G.  Tlio  glomeruli  stand  out  as  wliitisli 
(lots  and  the  sclerosed  arteries  are  easily  recognized,  as 
tlieir  Avails  are  iniieli  thickened.  The  process  does  not,  as 
a  rule,  affect  the  whole  kidney  equally,  but  rather  affects 
those  2>ortions  corresponding  to  the  interlohular  arteries. 
The  rej)laceinent  of  the  normal  kidney  tissue  by  connective 
tissue  and  the  resulting  contraction  of  this  latter  tissue 
leads  to  the  formation  of  scars.  As  the  process  is  not  reg- 
ular, the  scarring  is  deeper  in  some  places  than  in  others, 
with  the  result  that  localized  rather  sharply  depressed 
areas  appear  on  the  surface.  The  pelvis  is  relatively  large 
and  is  filled  with  fat.  The  renal  artery  is  often  markedly 
sclerosed  and  the  whole  process  may  be  due  to  localized 
thickening  of  the  artery,  or  as  part  of  a  general  arterioscle- 
rosis. The  latter  is  the  more  frequent.  Microscopically, 
it  is  seen  that  the  tubules  are  atrophied,  the  Bowman's 
capsules  are,  as  a  rule,  thickened,  and  the  glomeruli  are 
shrunken  or  have  l)een  rejjlaced  by  fibrous  tissue.  In  places 
they  have  fallen  out  of  the  section.  There  is  marked  i)ro- 
liferation  of  connective  tissue  in  cortex  and  medulla.  The 
arterioles  are  thickened,  the  sclerosis  l)eing  either  of  the 
intima  or  media  or  of  both.  There  is  even  occlusion  of 
many  arterioles. 

Changes  in  other  organs  as  the  result  of  arteriosclerosis 
of  their  afferent  vessels  occur,  but  are  not  so  characteristic 
as  in  the  kidney.  In  the  brain  the  result  of  gradual  thick- 
ening of  the  arterioles  is  a  diminished  blood  supply,  soften- 
ing of  the  portion  supplied  by  the  artery,  and  later  a  con- 
nective tissue  dej)Osit.  The  occurrence  of  thrombi  is  fa- 
vored and,  now  and  again,  a  thrombus  plugs  an  artery 
which  supplies  an  important  and  even  vital  part  of  the 
brain.  The  arteries  of  the  brain  are  end  arteries,  hence 
there  is  no  chance  for  collateral  circulation.  It  is  there- 
fore evident  how  serious  a  result  may  follow  the  disturb- 
ance in  or  actual  deprivation  of  blood  supj^ly  to  any  of  the 
brain  centers  or  to  the  internal  cai)sule. 


PATHOLOGY  63 

Arteriosclerosis  of  the  Pulmonary  Arteries 

There  liave  been  a  ]iu]nl)cr  of  eases  of  sclerosis  of  the 
puhiionary  arteries,  either  alone,  or  associated  with  general 
systemic  arteriosclerosis. 

A  primary  and  a  secondary  form  are  recognized,  the  for- 
mer in  conjunction  Avith  congenital  malformations  of  the 
heart,  the  latter  as  the  result  of  severe  infection  or  of  mi- 
tral stenosis.  These  two  causes  seem  to  be  the  most  imj)or- 
tant  in  the  production  of  the  arterial  changes.  The  cases 
thus  far  described  have  revealed  Avidespread  thickening 
of  the  pulmonary  arteries.  If  one  may  judge  by  the  de- 
scription of  the  pathologic  changes,  the  condition  is  cpiito 
similar  to  that  jiroduced  in  a  vein  l)y  transplantation  along 
the  course  of  an  artery.  The  diffuse  form  Avitli  connective 
tissue  thickening  of  all  coats  has  been  generally  described. 
There  is  also  obliterating  endarteritis  of  the  smaller  ves- 
sels. In  the  etiology  of  the  condition  severe  infection  seems 
to  play  a  prominent  role.  The  constant  presence  of  right 
ventricular  hypertrophy  is  interesting,  the  heart  dullness 
extends,  as  a  rule,  far  to  the  right  of  the  sternum.  In  some 
of  the  cases  no  demonstrable  changes  were  observed  in  the 
bronchial  arteries  or  in  the  pulmonary  veins. 

Sanders  has  descril)ed  a  case  of  primary  pulmonary  ar- 
teriosclerosis with  hypertrophy  of  the  right  ventricle. 

Recently  Warthin*  has  reported  a  case  of  syphilitic 
sclerosis  of  the  pulmonary  artery  Avhicli  i)laces  the  lesion 
in  exactly  the  same  category  as  that  of  syphilis  in  the  sys- 
temic arteries.  There  was  also  aneurysm  of  the  left  upper 
division  jjresent  and,  to  settle  the  etiologic  nature  of  the 
process.  Spirochete  pallida  were  found  in  the  wall  of  the 
aneurysm  sac  and  in  that  of  the  i3ulmonary  artery.  The 
microscopic  picture  in  the  pulmonary  artery  could  not  be 
told  from  that  in  a  syphilitic  aorta. 


*Warthin,  A.   S.  :     Am.  Jour.  Syph.,   1918,  i,  693. 


64  ARTERTOSCLEPvOSTS 

Sclerosis  of  the  Veins 

Plilebosclerosis  not  infrequently  occurs  witli  arterioscle- 
rosis. It  is  seen  in  those  cases  characterized  by  high  blood 
pressure.  Such  increased  pressure  in  the  veins  is  due,  for 
example,  to  cirrhosis  of  the  liver  which  affects  the  portal 
circulation,  or  to  mitral  stenosis  which  affects  the  pulmo- 
nary veins.  The  affected  vessels  are  usually  dilated.  The 
intima  shows  compensatory  thickening  especially  where  the 
media  is  thinned.  As  a  rule  all  the  coats  are  involved  in  the 
connective  tissue  thickening.  Occasionally  hyaline  degen- 
eration or  calcification  of  the  new-formed  tissue  is  seen. 
''Without  existing  arteriosclerosis  the  peripheral  veins 
may  be  sclerotic  usually  in  conditions  of  debility,  but  not  in- 
frequently in  young  persons."     (Osier.) 

In  many  cases  of  arteriosclerosis,  the  patliologic  changes 
are  not  confined  to  the  arteries,  but  are  found  in  the  veins 
as  well  as  in  the  capillaries.  Such  cases  could  be  called 
angiosclerosis. 


CHAPTER  III 

PHYSIOLOGY  OF  THE  CTPCULATTOX 

No  attempt  will  be  made  to  cover  the  entire  subject  of 
the  physiology  of  the  circulation.  Only  in  so  far  as  it  re- 
lates to  arteriosclerosis  and  blood  ])ressure  and  has  a  bear- 
ing on  the  probable  explanation  of  l)lood  pressure  phe- 
nomena will  it  be  discussed. 

"The  heart  and  the  blood  vessels  form  a  closed  vascular 
system,  containing  a  certain  amount  of  blood.  This  blood 
is  kept  in  endless  circulation  mainly  by  the  force  of  the 
muscular  contractions  of  the  heart;  l)ut  the  bed  through 
which  it  flows  varies  greatly  in  width  at  different  parts  of 
the  circuit,  and  the  resistance  offered  to  the  moving  blood 
is  very  much  greater  in  the  capillaries  than  in  the  large 
vessels.  It  follows,  from  the  irregularities  in  size  of  the 
channels  through  which  it  flows,  that  the  blood  stream  is 
not  uniform  in  character  throughout  the  entire  circuit — 
indeed,  just  the  opposite  is  true.  From  point  to  point  in 
the  branching  system  of  vessels  the  blood  varies  in  regard 
to  its  velocity,  its  head  of  pressure,  etc.  These  variations 
are  connected  in  part  with  the  fixed  structure  of  the  system 
and  in  part  are  dependent  upon  the  changing  properties  of 
the  living  matter  of  which  the  system  is  composed."  (W. 
H.  Howell.) 

If  the  vascular  system  were  composed  of  a  central  pump, 
projecting  at  every  stroke  a  given  amount  of  liquid  into 
a  series  of  rigid  tubes,  the  aggregate  cross  sections  of  which 
were  equal  to  the  cross  section  of  the  main  i)ipe,  then  the 
velocity  at  the  openings  would  be  the  same  as  at  the  source 
(making  allowances  for  friction).  The  problem  would  then 
be  a  simple  one.  In  the  circulation  of  the  blood  no  such 
simple  condition  obtains.    The  capillary  beds  is  an  enormous 

65 


()C)  AltTKIMOSCLETlOSIS 

ai'oa  tlii"()ii,i;li  wliieli  tlie  ])l()()d  flows  slowly.  From  the 
tiiiio  the  1)1()()(1  is  llirowii  into  the  aorta  the  velocity  begins 
to  diiHinish  until  it  reaches  its  minimum  in  the  capillaries. 
In  no  two  persons  is  the  initial  velocity  at  the  heart  the 
same,  nor  in  the  same  i)erson  is  it  the  same  at  all  times  of 
day.  The  size  of  the  heart,  the  actual  strength  of  the 
muscle,  the  amount  of  l)lood  ejected  at  every  beat,  and  the 
size  and  elasticity  of  the  aorta  are  some  of  the  factors  which 
determine  the  velocity  of  blood  at  the  aortic  orifice.  When 
to  these  factors  are  added  the  differences  in  arterial  tissue, 
the  activity  or  resting  stage  of  the  various  organs,  etc.,  the 
question  becomes  exceedingly  complicated.  In  spite  of 
these  many  disturl)ing  elements,  attempts  more  or  less  suc- 
cessful have  been  made  to  estimate  the  velocity  of  the  blood 
in  animals.  Thus,  in  the  carotid  of  the  horse  the  velocity 
was  found  to  be  oOO  mm.  per  second  (Volkman)  and  297 
nun.  (Chauveau);  in  the  carotid  of  the  dog,  260  mm. 
(Yierordt).  In  the  jugular  vein  of  the  dog  Vierordt  found 
the  velocity  to  be  225  mm.  per  second.  These  figures  do 
not  represent  the  actual  velocity  of  the  blood  in  all  horses 
or  all  dogs,  but  they  do  give  us  some  general  idea  of  the 
rate  of  fiow  of  the  blood.  For  man  it  has  been  calculated 
that  the  velocity  in  the  aorta  is  about  320  mm.  per  second. 
The  velocity  is  not  uniform  in  the  large  arteries,  where  at 
every  heart  beat  there  is  a  sudden  increase  followed  by  a 
decrease  as  the  heart  goes  into  diastole.  The  farther  aw^ay 
from  the  heart  the  measurements  are  made  the  more  even 
is  the  fiow. 

Observations  by  W.  H.  Luedde  with  the  Zeiss  binocular 
corneal  microscope  on  the  rate  of  flow  in  the  conjunctival 
capillaries  nmst  modify  somewhat  our  former  conceptions. 
He  finds  that  "The  rate  varies  in  the  different  arteries, 
capillaries,  and  veins  from  a  barely  perceptible  motion  to 
a  little  more  than  1  nnn.  per  second.  Further,  some  parts 
of  the  capillary  network  are  ordinarily  supplied  with  blood 
elements  only  occasionally.    This  is  shown  by  the  passage 


PHYSIOLOGY    OI'^    TITE    CUTU'l'LATlOX  67 

of  a  column  of  cori)iiscles  along  a  certain  lino,  follo^ved 
after  an  interval  of  seconds,  during  which  no  corpuscles 
pass,  by  another  column  in  the  same  line  as  before." 

The  vessels  of  the  conjunctiva  probalily  are  quite  like 
superficial  vessels  in  the  skin  and  mucous  membranes. 
Therefore,  we  must  be  free  to  admit  that  the  circulation 
in  them  is  not  absolutely  steady.  Luedde  found  further  that 
in  syphilitics  there  were  tortuosities,  irregularities,  minute 
aneurysmal  dilatations  and  even  obliterations  of  capillaries. 
Some  of  the  changes  occurred  as  early  as  one  month  after 
infection. 

The  rate  in  the  capillaries  of  man  is  estimated  to  be  be- 
tween 0.5  mm.  and  0.9  mm.  per  second.  As  the  blood  is 
collected  into  the  veins  and  the  bed  becomes  smaller,  the 
velocity  increases  until  at  the  heart  it  is  almost  the  same 
as  in  the  aorta.  That  the  velocity  could  not  be  exactly  the 
same  is  evident  from  the  fact  that  the  cross  section  of  the 
veins,  which  return  the  blood  to  the  right  auricle,  is  greater 
than  is  the  cross  section  of  the  aorta. 

The  volume  of  the  bed  is  subject  to  rapid  and  wide 
fluctuations,  which  are  dependent  on  many  causes,  both 
physiologic  and  i)athologic.  The  call  of  an  actively  func- 
tionating organ  or  group  of  organs  causes  a  widening 
of  a  more  or  less  extensive  area,  and  the  velocity  necessarily 
varies.  In  states  of  great  relaxation  of  the  vessels  there 
may  be  a  capillary  pulse.  In  order  to  force  blood  at  the 
same  rate  through  dilated  vessels  as  through  normal  ves- 
sels, there  must  be  more  blood  or  there  must  l)e  a  more 
rapid  contraction  of  the  central  pump.  What  actually 
happens,  as  a  rule,  is  an  increase  in  the  rate  of  the  heart 
beat.  There  are  conditions — such,  for  example,  as  aortic 
insufficiency — where  actually  more  blood  is  thrown  into 
the  circulation  at  every  beat,  so  that  the  rate  is  not 
changed. 

It  has  been  calculated  that  the  average  amount  of  blood 
thrown  into  the  aorta  at  everv  svstole  of  the  lieart  is  from 


68  AirrEii  loscLEiiosis 

50  to  100  c.c.  This  is  forcibly  ejected  into  a  vessel  already 
filled  (api)areiitly)  with  blood.  In  order  to  accommodate 
this  sudden  accession  of  fluid,  the  aorta  must  expand.  The 
aortic  valves  close,  and  during-  diastole  the  blood  is  forced 
through  the  vascular  system  by  the  forcible,  steady  contrac- 
tion of  the  highly  elastic  aorta.  Other  large  vessels  which 
branch  from  the  aorta  also  have  a  part  in  this  steady  pro- 
pulsion of  blood.  From  seventy  to  eighty  times  a  minute 
the  aorta  is  normally  forcibly  expanded  to  accommodate 
the  charge  of  the  ventricle.  It  is  not  difficult  to  under- 
stand the  great  frequency  of  patches  of  sclerosis  in  the  arch 
when  these  facts  are  borne  in  mind. 

What  relationship  the  viscosity  of  the  blood  has  to  the 
rate  and  volume  of  flow  is  not  fully  understood.  As  yet 
there  is  not  much  known  about  the  subject,  and  no  one  has 
devised  a  satisfactory  means  of  measuring  the  viscosity. 
It  is  thought  by  some  that  an  increased  viscosity  assists  in 
producing  an  increased  amount  of  work  for  the  heart. 

Blood  Pressure 

Blood  pressure  is  the  expression  used  for  a  series  of 
phenomena  resulting  from  the  action  of  the  heart.  As  every 
heart  l)eat  is  actual  w^ork  done  by  the  heart  in  overcoming 
resistance  to  the  outflow  of  blood,  this  force  is  approx- 
imately measurable  in  a  large  artery  such  as  the  brachial. 
It  has  been  determined  that  the  pressure  in  the  brachial 
artery  is  almost  equal  to  the  intraventricular  pressure  in 
the  left  ventricle.  In  animals  it  is  easy  to  attach  manom- 
eters to  the  carotid  artery  and  to  measure  the  ])lood  pres- 
sure accurately.  Formerly  the  method  consisted  in  attach- 
ing a  tube  and  allowing  the  blood  to  rise  in  the  tube.  The 
height  to  which  the  blood  rose  measured  the  maximum  pres- 
sure. This  is  a  crude  method  and  has  been  replaced  by 
the  U-tube  of  mercury  with  connection  made  to  the  artery 
by  saline  or  liinger's  solution.  This  apparatus  is  familiar 
to  all  physiologists. 


riivsioLO(;v  of  the  (.'Ihcl'latiox  G9 

In  man  the  measureniont  is  most  conveniently  made  from 
the  brachial  artery.  There  is  some  difference  in  the  pres- 
sure in  the  femoral  and  the  brachial  and  some  use  both 
arteries.  However,  the  difficulty  of  adjusting  instruments 
to  the  upper  leg,  the  great  force  which  must  be  used  to  com- 
press the  femoral  artery  and  the  relative  inaccessibility  of 
the  leg  as  compared  to  the  arm,  make  the  leg  an  inconveni- 
ent part  for  use  in  blood  pressure  determinations.  It  is 
not  to  be  recommended. 

Blood  pressure  is  a  valuable  aid  in  diagnosis  and  of  ma- 
terial help  in  many  cases  in  prognosis,  but  it  is  not  infalli- 
ble neither  can  it  be  used  alone  to  diagnose  a  case.  Blood 
pressure  is  only  one  of  many  links  in  a  chain  of  evidence 
leading  to  diagnosis.  It  has  been  badly  used  and  much 
abused.  It  has  been  condemned  unjustly  when  it  did  not 
furnish  all  the  evidence.  It  has  been  made  a  fetish  and 
worshipped  by  both  doctors  and  patients.  A  sane  concep- 
tion of  blood  ])ressure  must  be  widely  disseminated  lest 
we  find  it  being  discarded  altogether. 

Blood  pressure  consists  of  more  than  the  estimation  of 
the  systolic  pressure.  The  blood  pressure  picture  consists 
of  (1)  the  systolic  pressure,  (2)  the  diastolic  pressure,  (3) 
the  pulse  i)ressure  which  is  the  difference  between  the 
systolic  and  diastolic  pressure,  (4)  the  pulse  rate.  Ex- 
pressed in  the  literature  it  should  read  thus:  120-80-40;  72. 
That  tells  the  whole  story  in  a  brief,  accurate  form.  This 
is  recommended  in  history  reporting.  It  must  be  ever  kei)t 
in  mind  that  a  blood  pressure  reading  represents  the  work 
of  tlie  heart  at  the  nioineut  when  it  iras  falcii.  AVithiu  a 
few  minutes  the  pressure  may  vary  up  or  down.  There  is 
no  normal  pressure  as  such,  ])ut  an  average  pressure  for 
any  group  of  people  of  the  same  age  living  under  similar 
conditions.  The  habit  of  speaking  of  any  systolic  figure  as 
normal  should  l)e  broken.  A  i)ressure  i)icture  may  l)e  nor- 
mal but  a  systolic  reading,  whatever  it  may  be,  is  not  ac- 
curately designated  as  normal.  This  distinction  is  worth 
insisting  upon. 


<U  ARTElMOSCLEItOSIS 

Blood  Pressure  Instruments 

There  are  several  iiistruiiients  which  are  in  common  use 
for  the  purpose  of  recording-  l)lood  pressure  in  man. 

Historically,  the  determination  of  blood  ju'essure  for  man 
began  with  the  attempt  of  K.  Vierordt  in  1855  to  measure 
the  blood  pressure  by  placing  weights  on  the  radial  pulse 
until  this  was  obliterated.  The  first  useful  instrument, 
however,  was  devised  by  Marey  in  1876.  He  placed  the 
hand  in  a  closed  vessel  containing  water  connected  by  tub- 
ing with  a  l)()ttle  for  raising  the  pressure  and  by  another 
tube  with  a  taml)our  and  lever  for  recording  the  size  of  the 
pulse  waves.  He  maintained  that  when  pressure  on  the 
hand  was  made,  the  point  wdiere  oscillations  of  the  lever 
ceased  was  the  maximal  pressure,  the  point  where  the  oscil- 
lations of  the  recording  lever  was  largest,  was  the  minimal 
pressure. 

This  pioneer  work  was  practically  forgotten  for  twenty- 
five  years.  It  was  not  until  1887  that  Y.  Basch  devised  an 
instrument  Avhich  was  used  to  some  extent.  This  instru- 
ment recorded  only  maximum  ])ressure.  It  consisted  of  a 
small  ru])ber  bulb  tilled  with  water  communicating  with  a 
mercury  manometer.  The  bulb  w^as  pressed  on  the  radial 
artery  until  the  pulse  below  it  was  obliterated  and  the 
pressure  then  read  off  on  tlie  colunm  of  mercury.  V,  Basch 
later  substituted  a  spring  manometer  for  the  mercury 
colunm.  Potain  modified  the  apparatus  by  using  air  in  the 
l)ull)  with  an  aneroid  barometer  for  recording  the  pressure. 
These  instruments  are  necessarily  grossly  inaccurate. 
]\roreovei',  they  do  not  record  the  diastolic  pressure. 

In  1896  and  1897  further  attempts  were  made  to  record 
blood  i)ressure  by  the  introduction  of  a  flat  rubber  bag- 
encased  in  some  nonyielding  material,  which  was  placed 
around  the  upper  arm.  Riva-Iiocci  used  silk,  while  Hill 
and  Barnard  used  leather.  Qlie  latter  used  a  bulb  or 
Davidson  svringe  to  force  air  into  the  cuff  around  the  arm 


PJIVSIOLOCJV    OF    THE    C'lIH'L' LATIOX  71 

and  palpated  the  radial  artery  at  the  wrist,  iiotiii<>'  the  point 
of  return  of  the  pulse  after  compression  of  the  U])per  arm, 
and  reading  the  pressure  on  a  column  of  mercury  in  a  tube. 

Except  that  the  width  of  the  cuff  has  been  increased  from 
5  cm.  to  12  cm.,  this  is  the  general  principle  upon  which  all 
the  blood  pressure  instruments  now  in  use  are  l)ased. 
]\rost  of  the  apparatuses  make  use  of  a  column  of  mercury 
in  a  U-tube  to  record  the  millimeters  of  pressure.  As  the 
mercury  is  depressed  in  one  arm  to  the  same  extent  as  it 
is  raised  in  the  other  arm  the  scale  where  readings  are  made 
is  .5  cm.  and  the  divisions  represent  2  mm.  of  mercury  but 
are  actually  1  mm.  apart. 

The  cuff  was  made  12  cm.  in  diameter  because  it  was 
shown  (v.  Recklinghausen)  that  with  narrow  cuffs  nmch 
pressure  was  dissipated  in  squeezing  the  tissues.  Jane- 
way  has  shown  that  with  the  use  of  the  12  cm.  cuff 
accurate  values  are  obtained  independently  of  the  amount 
of  muscle  and  fat  around  the  brachial  artery.  In  other 
words  if  an  actual  systolic  blood  pressure  of  140  nun.  is 
present  in  two  individuals,  the  one  with  a  thin  arm,  the 
other  with  a  thick  arm,  the  instrument  will  record  these 
pressures  the  same  where  a  12  cm.  arm  band  is  used.  We 
need  have  no  fear  of  obtaining  too  high  a  reading  when 
we  are  taking  pressure  in  a  stout  or  very  nmscular  individ- 
ual. Janeway  also  was  the  first  to  call  attention  to  the  fact 
that  the  diastolic  or  minimal  pressure  was  at  the  point 
wdiere  the  greatest  oscillation  of  the  mercury  took  place. 
This  is  difficult  to  estimate  in  many  cases  as  the  eye  can 
not  follow  slight  changes  in  the  oscillation  when  tlie  i)res- 
sure  in  the  cuff  is  gradually  reduced.  Practically  this  is 
the  case  in  small  pulses. 

The  Riva-Rocci  instrument  was  modified  l)y  Cook.  (See 
Fig.  13.)  He  used  a  glass  bulb  containing  mercury  into 
which  a  glass  tube  projected.  The  bulb  was  connected  by 
outlet  and  tubing  to  the  cuff  and  syringe.  The  glass  tube 
"svas  marked  off  in  centimeters  and  millimeters  and  for  con- 


i'^ 


AKTKHIOSCLEIIOSIS 


vciiiciicc  was  joiiittMl  lialT  way  in  its  l('ii,<''tli.  ''i^hc  iiistini- 
iiR'iit  C!)iild  1)0  carried  in  a  box  of  convenient  size.  This 
instrument  is  fragile  and  more  cumbersome,  altlioug"li 
lighter  in  weight,  than  others  and  is  very  little  used  at 
present. 

Stanton's  instrument  (Fig.  14)  is  i)ractically  Cook's 
made  more  rigid  in  every  way  but  without  the  jointed  tube. 
The  cuff  has  a  leather  casing,  the  pressure  bulb  is  of  heavy 
rubber,  the  (ilass  tul)e  in  which  the  mercurv  rises  is  fixed 


Imi;.     13. — C(j()k's    nuKtilication    of    Uiva-Rocci's    blood    i)rcssiii-(.-    instruiiKMit. 

against  a  piece  of  flat  metal  and  there  are  stopcocks  in  a 
metal  chamber  introduced  between  the  bulb  and  mercury 
with  which  to  regulate  the  in-  and  out-flow  of  air.  The 
pressure  can  i)e  gradually  lowered  conveniently  without  re- 
moving the  pressure  bulb. 

The  most  accurate  mercury  manometer  is  that  of  Er- 
langer.  (Fig.  15.)  Tlie  instrument  is  bulky  and  is  not 
jiracticable  for  the  physician  in  practice.  The  principle  is 
that  used  bv  Kiva-Kocci.     There  is  an  extra  T-tube  intro- 


PlIVSlOLOdY    OF    THE    ClItCri.ATIOX 


<o 


duced  between  the  manometer  and  air  bulb  connecting  with 
a  rubber  bulb  in  a  glass  chamber.  The  oscillations  of  this 
are  communicated  to  a  Marey  tambour  and  recorded  on 
smoked  paper  revolving  on  a  drum.  There  is  a  compli- 
cated valve  which  enables  the  operator  to  reduce  the  pres- 
sure with  varying  degrees  of  slowness.  The  mercury  is 
placed  in  a  U-tube  with  a  scale  alongside  it.  The  instru- 
ment is  expensive  and  not  as  easy  to  manipulate  as   its 


l'"ig.    14. — Stanton's    spli)  ^jnionianumctcr. 

advocates  would  have  us  believe.  Hirschfelder  has  added 
to  the  usefulness  (as  well  as  to  the  complexity)  of  the  Er- 
langer  instrument,  by  placing  two  recording  tambours  for 
the  simultaneous  registering  of  the  carotid  and  venous 
pulses.  In  spite  of  its  complexity  and  necessary  bulkiness, 
very  valuable  data  are  obtained  concerning  the  auricular 
contractions. 


74 


ARTERIOSCLEROSIS 


One  of  the  best  of  the  mercury  instruments  is  the  Brown 
si)hyg'm(mianometer.  In  this  (Fig.  16)  the  mercury  is  in 
a  closed,  all-ghiss  tube  so  that  it  can  not  spill  under  any 


Fig.  13. — The  Erianger  sphyginoiiianometer  with  the  Uirschfelder  attachtncnts  by 
means  of  which  simultaneous  tracings  can  be  obtained  from  the  brachial,  carotid,  and 
venous  pulses. 


PHYSIOLOGY    OF    THE    CJUCI'LATIOX 


Vi) 


sort  of  manipulation.  It  is  in  this  sense  ''fool-proof."  The 
cuff,  however,  is  poorly  constructed.  It  is  too  short  and 
there  are  strings  to  tie  it  around  the  arm.  I  have  found 
that  this  causes  undue  pressure  in  a  narrow  circle  and  ren- 


Fig.    16. — Desk    model     liauiiiaiiiinii.ti 


ders  the  reading  inaccurate.  In  the  clinic  we  use  this  mer- 
cury instrument  with  a  long  cuff  like  that  provided  by  the 
Tycos  instrument. 

The   Faught   instrument    (Fig.  17)    is   larger   than   the 
Brown,  but  is  less  easily  broken  and  is  not  too  cumbersome 


76 


AltTEUlOSCLEItOSIS 


to  carry  around.  The  substitution  of  a  metal  air  i)ump  for 
the  rubber  makes  the  apparatus  more  durable. 

The  V.  Rockling'hausen  instrument  is  not  employed  to 
any  extent  in  this  country.  It  is  both  expensive  and  cum- 
bersome, and  has  no  advantages  over  the  other  instruments. 

Several  other  instruments  have  been  devised  and  new  ones 
are  constantly  being  added  to  the  already  large  list.  With 
those  emx)loying  mercury  the  principle  is  the  same.  The 
aim  is  to  make  an  instrument  which  is  easily  carried,  dura- 
ble, and  accurate. 

In  all  the  mercurv  instruments  the  diameter  of  the  tube 


I'ig.     17. — The     Vauglit    blood    pressure    instruiiK'nt.       An     excellent     instrnnient     which     is 
(luife    easilj'    carried    abont    and    is    not    easily    broken. 

is  2  mm.  One  would  sui)pose  that  there  would  be  notice- 
able differences  in  tlie  readings  of  the  ditferent  mercury 
instruments  depending  upon  the  amount  of  mercury  used 
in  the  tube.  By  actual  weight  there  is  from  35  to  45  gnis. 
of  mercury  in  the  several  instruments.  After  many  trials, 
no  noticeable  differences  in  blood  pressure  readings  can  be 
made  out  between  a  column  weighing  85  gm.  and  one  weigh- 
ing 45  gm. 

There  is,  however,  the  inertia  of  the  mercury  to  be  over- 


PHYSIOLOGY    OF    THE    CIRCULATIOX 


i  ( 


conio,  fi'ictioii  botweon  the  tube  and  the  mercury,  and  vapor 
tension.  The  mercury  is  tlierefore  not  as  sensitive  to  rapid 
changes  of  i)ressure  in  the  cuff  as  a  lighter  fluid  would  be. 
The  mercury  must  be  clean  and  the  tube  dry  so  that  there 
is  no  more  friction  than  what  is  inherent  between  the  mer- 
cury and  glass.  In  making  readings  on  a  rapid  pulse  the 
oscillations  of  the  mercury  column  are  apt  to  be  irregular 
or  to  cease  now  and  then,  due  to  the  fact  that  the  downward 
oscillation  coincides  with  a  pulse  wave,  or  an  upward  oscil- 
lation receives  the  impact  of  two  pulse  waves  transmitted 
through  the  cuff.  Instruments  have  been  devised  to  obviate 
this  difficulty,  but  they  have  not  come  into  favor.    They  are 


Fig.    IS. — Rogers'    "Tycos"    dial    s|)liy.enKinian()iiictcr. 

usually  too  conii)licated  and  at  present  can  not  be  recom- 
mended. 

An  instrument  devised  by  Dr.  Eogers  (the  '^ Tycos") 
has  met  with  considerable  popularity.  (Fig.  18.)  This  is 
not  an  instrument  which  operates  with  a  spring  and  lever. 
The  instrument  is  composed  essentially  of  two  metal  discs 
carefully  ground  and  attached  at  their  circumferences  to 
the  metal  casing  below  the  dial.  There  is  an  air  chamber 
between  these  discs  through  the  center  of  which  air  is 
forced  by  the  syringe  bulb.  "When  air  is  forced  into  the 
space  between  these  two  discs,  they  are  forced  apart  to  a 
very  slight  extent,  with  the  highest  pressures  only  2-3  mm. 
of  bulging  occurs.    From  data  gathered  after  extensive  use 


(Q  ARTERIOSCLEROSIS 

for  five  years  these  discs  were  not  found  to  have  sprun|^. 
A  k'ver  attached  to  a  cog  wliich  in  turn  is  attached  to  the 
dial  needle  magnifies  to  an  enormous  extent  the  slightest 
expansion  of  the  discs.  Every  dial  is  handmade  and  every 
division  is  actually  determined  by  using  a  U.  S.  govern- 
ment mercury  manometer  of  standard  type.  Xo  two  dials 
therefore  are  alike  in  the  spacing  of  the  divisions  of  the 


Fig.    19. — Detail  of  the  dial   in  the   "Tycos"'   instrument. 

scale  but  every  one  is  calibrated  as  an  individual  instru- 
ment. There  is  no  doubt  in  the  author's  mind  that  for  the 
general  practitioner  the  instrument  has  some  advantages 
over  the  mercury  instruments.  It  reveals  the  slightest 
irregularity  in  force  of  the  heart  beat.  The  oscillation  of 
the  dial  needle  is  more  accurately  followed  by  the  eye  than 
is  that  of  the  column  of  mercury.  The  needle  passes  di- 
rectly over  the  divisions  of  the  scale,  while  with  usual  mer- 


PHYSIOLOGY    OF    THE    CIRCULATIOX 


'9 


cury  instruments  the  scale  is  an  appreciable  distance  (some- 
times .5  cm.)  from  the  column  of  mercury  at  the  side.  (Fig. 
19.)     The  diastolic  pressure  is  more  easily  read  on  the 


Fig.    20. — I'auglit    dial    instnuiient. 


Fig.  21. — Detail  of  the  dial  of  the  Faiight  instrument. 


so 


APiTEniOSCLEROSIS 


''Tycos. "  It  is  where  the  maximum  oscillation  of  the  nee- 
dle occurs  as  the  pressure  is  slowly  released  from  the  cuff. 
Althoug'h  it  does  not  appear  that  this  instrument,  if  prop- 
erly made  and  standardized,  could  become  inaccurate, 
nevertheless  it  is  advisable  to  check  it  every  few^  months 
against  a  known  accurate  mercury  manometer  instrument. 

Anotlier  perfectly  satisfactory  dial  instrument  is  the 
Fauglit  (Figs.  20  and  21).  The  general  plan  of  this  differs 
in  some  minor  points  from  the  "Tycos."  T  have  compared 
tlie  two  and  have  found  no  difference  in  the  readings.  Both 
can  l)e  recommended. 

One  or  two  other  cheaper  dial  instruments  are  on  i.he 
market.    The  Sanborn  seems  to  ])e  quite  satisfactory.    (Fig. 


Fig. 


-The    San1)orn    instrument. 


22.)  It  is  cheaper  than  the  other  dial  instruments.  There 
is  this  much  to  be  said,  no  instrument  using  a  spring  as  re- 
sistance to  measure  joressure  can  be  recommended. 


Technic 

The  same  teclmic  applies  to  all  the  mercury  instruments. 
The  patient  sits  or  lies  down  comfortably.  The  right  or  left 
arm  is  bared  to  the  shoulder,  the  cuff  is  then  slipped  over 
the  hand  to  the  upper  arm.  (See  Fig.  23.)  At  least  an  inch 
of  bare  arm  should  show  between  the  lower  end  of  the  cuff 
and  the  l)end  of  tlie  ell)OW.  The  rubber  is  adjusted  so  that 
tlie  actual  pressure  from  the  l)ag  is  against  the  inner  side 


PHYSIOLOGY    OF    THE    CUtCULATlOX 


81 


of  tlie  arm.  The  straps  are  tightened,  care  being  taken  not 
to  compress  tlie  veins.  Tlie  upper  part  of  the  cnff  slioukl 
fit  more  snugly  than  the  lower  part.  The  part  of  the  in- 
strument carrying  the  inercury  colunm  is  now  placed  on  a 
level  surface;  the  two  arms  of  the  mercury  in  the  tul)e  nmst 
be  even,  and  at  0  on  the  scale.  AVitli  the  fingers  of  one  hand 
on  the  radial  jjulse,  the  bag  is  compressed  until  the  pulse 
is  no  longer  felt.  (See  Fig.  24.)  One  should  I'aise  the  pres- 
sure from  10-12  mm.  al)()ve  this,  and  close  the  stopcock 


Vig. 


-Metlinrl    of    taking   blood    iirt'ssurt-    with    a    patient    in    sitting   j'osition. 


between  the  bulb  and  the  mercury  tube.  In  a  good  instru- 
ment the  colunm  should  not  fall.  If  it  does  there  is  a  leak 
of  air  in  the  system  of  tubing  and  arm  bag.  Xow  with  the 
fmger  on  the  pulse,  or  where  the  ])ulse  was  last  felt,  grad- 
ually allow  air  to  escape  by  turning  the  stoju-ock  so  that 
the  colunm  of  mercuiy  falls  about  2  nmi.  (one  division  on 
the  scale)  for  every  heart  beat  or  two.  One  must  not  allow 
the  colunm  of  mercurv  to  descend  too  slowlv  as  it  is  un- 


82 


AltTKItlOSCLEROSIS 


coiiil'ortahlc  for  llic  j)atieiit  aiul  introduces  a  ])sycliic  elc- 
luont  of  annoyance  wliicli  affects  the  l)lood  pressure.  On  the 
otlier  liand,  the  pressure  must  not  l)e  released  too  rapidly, 
else  one  i-uns  over  the  points  of  systolic  and  diastolic  pres- 
sui'e  and  tlie  readiii,sj,s  ai'e  ,L!,'rossly  inaccui-ate.  It  is  impossi- 
l)le  to  say  how  i-apidly  the  inei'cury  nuist  fall.  Every  opera- 
tor nuist  find  that  out  for  iiimself  by  practice.  The  first  per- 
cepti))le  i)idse  wave  felt  l)eneath  the  palpating-  finger  at  the 
wrist,  represents  on  the  scale  the  systolic  pressure.  This 
can  1)0  seen  to  coi'respond  to  a  sudden  increase  in  the  niagni- 


]•*!«.    24.  —  Mc-tlic)(l    (if    takiiiR    lilnod    pressure    with    patient    lying    down. 


tude  ol*  the  oscillation  ol'  the  niercui'V  colunni.  The  systolic 
I^ressure,  thus  ol)tained,  is  fi-oni  5-10  nnu.  lower  tlian  the 
real  systolic  ])i'essure.  ''I'he  nioi'e  sensitive  the  pa]i)ating- 
linger,  the  more  neai'ly  does  the  systolic  pressure  reading 
approacli  that  found  I)y  using  such  an  insti'uuient  as  Ei*- 
langer's,  whei'e  the  first  ])ulse  wave  is  magnified  l)y  the 
lever  of  the  taml)our. 

The  i)ressure  is  now  allowed  to  fall,  until  the  palpating 


PHYSIOLOGY    OF    THE    CIRCULATIOX  83 

finger  feels  the  largest  possible  i)ulse  wave,  \\iiicli  is  coinei- 
■deiit  with  the  greatest  oscillation-  of  the  niereiiry.  This  is 
the  diastolic  pressure.  Beyond  this  point  there  is  no  oscil- 
lation of  the  mercury  column.  The  difference  between  the 
two  is  the  pulse  pressure.  Thus  the  pulse  is  felt  after  com- 
pression at  120  on  the  scale,  and  the  maximum  oscillation 
occurs  at  80.  The  systolic  pressure  is  120  nun.,  tlie  dias- 
tolic is  80  mm.,  and  the  pulse  pressure  is  40  nnn. 

AVith  the  "Tycos"  or  Fauglit  the  arm  l)and  is  snugly 
wound  around  the  arm,  the  bag  next  to  the  skin  and  the  end 
tucked  in,  so  that  the  whole  band  will  not  loosen  when  air 
is  forced  into  the  l)ag.  The  cuff  is  ])lown  up  until  the  pulse 
is  no  longer  felt.  One  should  raise  the  pressure  not  more 
than  U)  mm.  above  the  point  of  obliteration  of  the  i)ulse. 
The  valve  is  then  carefully  opened  so  that  the  needle  grad- 
ually turns  toward  zero.  At  the  first  return  of  the  pulse 
wave  felt  at  the  wrist,  the  needle  is  sure  to  give  a  sudden 
jump.  This  is  the  systolic  pressure  and  is  read  off  on  the 
scale.  The  ne(^dle  is  now  cai'efully  watched  until  it  shows 
the  maximum  oscillation.  This  is  the  diastolic  pressure. 
The  dilYerence  between  the  two  is,  as  above,  the  pulse  pres- 
sure. 

In  taking  pressure  one  should  take  the  average  of  several, 
tlu'ee  or  four.  Moreover,  one  nmst  not  take  consecutive 
readings  too  quickly  and  one  must  be  sure  that  between 
every  two  readings  all  the  air  is  out  of  the  cuff  and  that  the 
mercury  or  dial  is  at  zero.  It  has  been  fepeatedly  shoivn 
fliat  in  a  cijanosed  arm  the  fiijstotic  pressure  is  raised  so 
that  even  stight  eijanosis  hetireen  readings  must  he  eare- 
fnlti)  avoided. 

The  only  accurate  method  of  determining  both  the  sys- 
tolic and  diastolic  jiressure,  l)ut  especially  the  diastolic,  is 
l)y  the  so-called  auscultatory  method.  (See  P'ig.  2.").)  The 
cuff  is  adjust(Hl  in  the  usual  way  and  one  places  the  bell 
of  a  binaural  stethoscope  over  the  brachial  artery  from 
one    to    two    centimeters    below    the    lower    edu'e    of    the 


84 


ARTEIlTOSCLEROSrS 


cuff.*  Care  niiist  be  taken  tliat  tlie  ])ell  is  not  pressed  too 
firmly  afj;ainst  tlie  arm  and  tliat  tlie  edge  of  tlie  bell  nearest 
the  cuff  is  not  pressed  more  firmly  than  the  opposite  end. 
For  this  purpose,  one  can  not  use  the  ordinary  l^owles 
stethoscope  or  any  of  the  other  much  lauded  steth- 
oscopes, because  the  surface  of  the  ])ell  is  too  large.  The 
diameter  of  the  bell  must  not  l)e  more  than  twenty-five  mil- 
limeters, twenty  is  still  better.  It  is  advisal^le  before  l)e- 
g-inning  the  observation  to  locate  with  the  finger  the  pulse 


Fi«. 


-Oljservation  by   the   auscultatory   method   and   a   mercury   instrument.      One   hai 
regulates   the    stop    cock    whicli    releases    air    gradually. 


ill  the  brachial  artery  just  above  the  elbow,  so  that  the 
stethoscope  may  be  placed  over  the  course  of  the  artery. 
(Fig.  26.)  The  first  wave  which  comes  through  is  heard  as 
a  click,  and  occurs  at  a  point  on  the  manometer  or  dial  scale 
from  5-10  mm.  liigher  than  can  usually  be  palpated  at  the 
radial  artery.    This  is  the  true  systolic  pressure.    By  keep- 


*A   firm  makes  a  stethoscope  so  that  the   bell  is  clami)cd  on   the   arm   leaving  both   the 
operator's  hands   free. 


PHYSIOLOGY    OF    THE    CIRCULATION 


85 


iiig  the  bell  of  the  stetlioscope  over  the  ])rac'liial  artery 
while  the  pressure  is  falling,  one  comes  to  a  point  wlien  all 
sound  suddenly  ceases.  This  is  said  to  be  the  diastolic  pres- 
sure.   This  is  incorrect  as  will  be  shown  later. 


I'ig. 


-Observation    by    the    auscultatory    method    and    a    dial    instrument.       Tlie    right 
hand    holds   the   bulb   and    regulates   the    air    valve. 


Arterial  Pressure 

Tlie  arterial  pressure  in  the  large  arteries  undergoes  ex- 
tensive fluctuations  with  every  heart  beat.  The  maxiniuni 
pressure  produced  by  the  systole  of  the  left  ventiicle  of  the 
heart  is  known  as  the  maximum  or  systolic  pressure.  It 
practically  equals  the  intraventricular  jn'essure.  The  niini- 
numi  pressure  in  the  artery,  the  in'essure  at  the  end  of  dias- 
tole, is  called  the  diastolic  pressure.  The  difference  ])e- 
tween  the  systolic  and  diastolic  xjressures  is  known  as  the 
pulse  pressure.  There  is  yet  another  term  known  as  the 
mean  pressure.    For  convenience,  this  may  be  said  to  be  the 


8G 


AIlTEiriO.SCLElIOSIrf 


aritliMiolic'dl  mean  of  tlie  systolic  and  diastolic  pressures. 
Actually,  liOwever,  this  can  not  be  the' case,  owing  to  the 
form  of  the  pulse  wave,  which  is  not  a  uniforiii  rise  and  fall 
- — the  ujistroke  ])eing  a  straight  line,  hut  the  doWnstroke  be- 
ing broken  usually  ])y  two  iu)tches.  AVe  do  not  make  use  of 
the  mean  pressure  in  recording  results.  It  is  of  experimen- 
tal interest  and  needs  only  to  be  mentioned  here. 

It  has  been  shown  that  the  mean  pressure  is  quite  con- 
stant throughout  the  whole  arterial  system.  Tlie  maximum 
pressure  necessarily  falls  as  the  periphery  of  the  vascular 
system  is  approached.     In  general  it  may  be   said  that 


.  Fig.  27. — Sclienia  lo  illustrate  the  gradual  decrease  in  pressure  from  the  heart  to  the 
vena  cava:  (a),  arteries;  (c),  cainllaries;  (v),  veins;  (.\),  aorta,  pressure  l.SO  mm.; 
(1)),  brachial  artery,  pressure  1,H0  mm.;  (F),  femoral  vein,  20  mm.;  (I\'C),  inferior 
vena   cava,    3    mm.      (Modified    from    Howell.) 


the  minimal  pressure  is  quite  constant.  Too  little  attention 
is  paid  to  minimal  and  pulse  pressure.  The  minimal  pres- 
sure is  inqjortant,  for  it  gives  us  valuable  data  as  to  the 
actual  propulsive  force  driving  the  blood  forward  to  the 
})eriphery  at  the  end  of  diastole. 

It  is  readily  understood  how  the  maxinuun  pressure  falls 
as  the  periphery  is  approached,  until  in  the  arterioles  the 
maxinuim  and  inininuuh  pressures  are  about  equal.  The 
pressure  then  in  these  arterioles  is  practically  the  same  as 
the  diastolic  pressure.  Actually  it  is  a  few  millimeters 
less.  The  diastolic  blood  pressure  would,  therefore,  meas- 
ure the  peripheral  resistance  and,  as  the  maxinuim  for 
systolic  pressure  represents  approximately  the  intraven- 


rilYSIOLfXiV    OF    THE    ClItCULATIOX  87 

tricular  pressure,  tlie  diifereiiee  between  tlie  two,  the  pulse 
pressure,  actually  represents  the  force  which  is  drivino-  the 
blood  onward  from  the  heart  to  the  periphery.  It  is  lience 
very  evident  that  the  mere  estimation  of  the  systolic  pres- 
sure gives  us  but  a  i)ortion  of  the  iirformation  we  are 
seeking. 

The  jmlse  pressure  is  subject  to  wide  fluctuations  l)ut  as 
a  rule  for  any  one  normal  lieart  it  remains  fairly  constant 
as  the  rate  varies.  In  a  rapidly  beating  heart  the  diastole 
is  short  and  the  diastolic  pressure  rises.  If  the  systolic 
pressure  does  not  also  rise,  as  in  a  normal  heart  following 
exercise,  we  will  say,  the  j)ulse  pressure  falls.  AV(^  know 
that  when  the  pulse  rate  is  constant,  vasodihitation  causes  a 
fall  in  diastolic  pressure  and  a  rise  in  i)ulse  ])ressure.  On 
the  contrary,  vasoconsti'iction  causes  a  rise  in  diastolic 
pressure  and  a  fall  in  pulse  pressure. 

It  is  very  i)robably  the  case  that  with  two  individuals  of 
equal  age  and  equal  pulse  rate,  and  equal  systolic  pressure 
of  160  mm.,  the  oue  with  a  diastolic  pressure  of  110  mm. 
and,  therefore,  a  pulse  pressure  of  50  mm.  is  much  worse 
off  than  the  other  with  a  diastolic  pressure  of  90  nun.  and  a 
pulse  pressure  of  70  nnu.  The  latter  may  l)e  noi-mal  for  the 
age  of  the  person  especially  when  certain  forms  of  fibrous 
arteriosclei'osis  accompanied  by  enlarged  heart  are  present. 

The  former  is  not  normal  for  any  age.  I.ow  pulse  ])res- 
sure  usually  means  a  weak  vasomotor  control  and  is  only 
found  in  failing  circulation  or  in  markedly  i-un  do^\^l  states, 
such  as  after  serious  illness  or  in  tu1)ercul()sis.  Therefore, 
it  is  most  important  to  estimate  accurately  the  diastolic 
pressure  as  well  as  the  systolic  pressui-e,  foi-  only  in  this 
way  can  we  obtain  any  data  of  value  regarding  the  driving- 
power  of  the  heart  and  the  condition  of  the  A^asouiotor  sys- 
tem. A  high  systolic  pressure  does  not  necessarily  mean 
that  a  gr(»at  deal  of  blood  is  forced  into  the  ca])illaries.  Ac- 
tually it  may  mean  that  very  little  l)l()()d  entcis  the  ])('ri))h- 
erv.    The  heai't  wastes  its  streniith  in  dilating  constrict(Ml 


88  AKTKItlOSCI.KltOSIS 

vessels  witliout  actually  ('arryiii_i>'  on  the  circulatioii  ado- 
(|uati'ly. 

Normal  Pressure  Variations 

The  systolic  ])rcssu]'(3  varies  considerably  iiiider  condi- 
tions wliicli  are  by  no  means  abnoi'nial.  Thus,  tlie  average 
for  men  at  all  ages  is  al)out  127  nun.  llg.  (All  measure- 
ments are  taken  from  the  bracliial  artery,  with  the  individ- 
uals in  the  sitting  postnre.)  For  women  the  average  is 
somewhat  lower,  120  mm.  Hg.  The  jjressure  is  lowest  in 
children.  In  cliildi'en  from  G-12  years  the  average  systolic 
l)ressure  is  112  min.  Xormally,  there  is  a  gradual  increase 
as  age  conies  on,  due,  as  will  be  shown  in  the  succeeding 
chai)ter,  to  physiologic  changes  wliicli  take  j^lace  in  the 
artei'ies  from  birth  to  old  age.  In  tlie  chart  here  ai:)pended 
is  graphically  shown  the  normal  variations  in  the  l)lood 
l)ressure  at  different  ages  compiled  from  observations  made 
on  one  thonsand  presumal)ly  normal  persons.     (Fig.  28.) 

The  diastolic  pressnre  has  been  estimated  to  be  abont  35 
to  45  nun.  llg  lower  than  the  systolic  pressure,  and  conse- 
quently these  ligui'es  repi'esent  the  j^ulse  ])ressure  in  the 
brachial  ai'tery  of  man.  This  is  equivalent  to  saying  that 
every  systole  of  the  left  ventricle  distends  this  artery  by  a 
sudden  increase  in  pi-essure  equal  to  the  weight  of  a  colunm 
of  mercury  2  mm.  in  diametei-  and  35  to  45  mm.  high.  Xat- 
urally,  at  the  heart  the  pi'essure  is  highest.  As  the  blood 
goes  toward  the  capillary  ai'ea  the  pressure  gradually  de- 
creases until,  at  the  openings  of  the  great  veins  into  the 
heart,  the  i)ressure  is  least.  At  the  aorta  (A)  the  pi-essure 
(systolic)  is  ai)i)roxiinately  150  nun.  llg,  at  the  l)rachial 
artery  (B)  it  is  130  nun.,  in  the  capillary  system  (C)  it  is 
30  nun.,  in  the  femoral  vein  (F)  it  is  20  nun.,  at  the  opening 
of  the  inferior  vena  cava  (1)  it  is  3  nun. 

Attention  has  been  called  to  the  nonnal  systolic  pressure 
at  different  ages.  'I'his  is  not  the  only  cause  for  variations 
in  the  blood  pressure,    Xoi-mally,  it  is  givater  wheji  in  the 


PHYSIOLOGY   OF   THE    CIRCULATIOX 


89 


erect  position  than  wlien  seated,  and  greater  wlien  seated 
tlian  when  lying  down.  During  the  day  tliere  are  well- 
recognized  clianges.  The  pressure  is  lowest  during  the 
early  morning  lioui's,  when  the  person  is  asleejD.  In  women 
there  are  variations  due  to  menstruation.     Muscular  exor- 


ACTES 


mm 

1B0 

16  TO  30 

30  TO  40, 

40  TO  50 

50  TO  60     ] 

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143 
142 
141 
140 

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138 
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" 

I'ig.   28. — Chart   showing  the   normal   limits   of  variation   in   sv.stolic   blood   iircssurc       (  Aftir 

Woley.) 

cise  raises  the  blood  pressure  markedly.  The  effect  of  a 
full  meal  is  to  raise  the  blood  pressure.  The  explanation 
is  that  during  and  following  a  meal  tliere  is  dilatation  of 
the  abdominal  vessels.  This  takes  ])lood  from  other  parts 
of  the  body,  provided  that  the  other  factors  in  the  circula- 


90  :        .  AKTEItlOSCLEltOrill^   -  ■ 

tioii  remain  coiistaiit.  A  fall  of  ])ressiire  would  nceDK.sarily 
occur  in  the  aoi-ta.  To  compensate  for  tliis,  there  is  in- 
creased woi'k  on  tlie  part  of  tlie  lieart,  whicli  reveals  itself 
as  increased  pressure  and  pulse  pressure.  It  is  well  known 
that  the  interest  in  the  jji'ocess  taken  by  an  individual  upon 
whom  the  blood  pressure  is  estimated  for  the  first  time  tends 
to  increase  the  rate  of  the  heart  and  to  raise  the  blood  pres- 
sure. For  this  reason  the  first  few  readings  on  the  instru- 
ment must  be  discarded,  and  not  until  the  patient  looks 
upon  the  procedure  calmly  can  the  true  blood  pressure  be 
obtained.  As  a  corollary  to  this  statement,  mental  excite- 
ment, of  whatever  kind,  has  a  marked  influence  on  the 
pressure.  The  patient  nuist  remain  absolutely  quiet,  liais- 
ing the  head  or  the  free  arm  causes  the  pressure  to  rise. 
Another  imi)ortant  physiologic  variation  is  produced  by 
concentrated  inental  activity.  This  tends  to  hurry  the  lieart 
and  increase  the  force  of  the  beat.  In  short,  it  may  be 
stated  as  a  general  rule  that  any  active  functioning  of  a 
part  of  the  body  which  naturally  requires  a  great  excess  of 
blood  tends  to  elevate  the  blood  pressure.  At  rest  the  pres- 
sure is  constant.  Variations  caused  by  the  factors  men- 
tioned act  only  transitorily,  and  the  pressure  shortly  re- 
turns to  normal. 

The  Auscultatory  Blood  Pressure  Phenomenon 

Since  the  first  description  of  the  auscultatory  blood  pres- 
sure sounds  by  Korotkov  in  1905,  this  method  has  been  more 
and  more  employed  until  today  it  is  the  standard,  recog- 
nized method  of  determining  the  points  in  the  blood  j^res- 
sure  reading.  When  one  applies  the  12  cm.  arm  band  over 
the  brachial  artery  and  listens  with  the  bell  of  the  stetho- 
scope about  one  cm.  below  the  cuff  directly  over  the  lira- 
chial  artery  near  the  bend  of  the  elbow,  one  hears  an  inter- 
esting series  of  sounds  when  the  air  in  the  cuff  is  gradually 
]-educed.  The  cuff  is  blown  up  a])ove  the  maxinunn  pres- 
sure.    As  the  air  pressure  around  the  arm  gradually  is 


PHYSIOLOGY    OF    THE    CIRCULATION  91 

lowered,  the  series  of  sounds  begins  with  a  rather  h)w- 
pitched,  clear,  clicking  sound.  This  is  the  first  phase.  This 
only  lasts  through  a  few  millimeters  fall  when  a  murmur 
is  added  and  the  tone  becomes  louder.  This  click  and  mur- 
mur phase  is  the  second  phase.  A  few  millimeters  more  of 
drop  in  pressure  and  a  clear,  sharp,  loud  tone  is  audil)le. 
Usually  this  tone  lasts  through  a  greater  drop  than  any  of 
the  other  tones.  This  is  the  third  phase.  Rather  suddenly 
the  loud,  clear  tone  gives  place  to  a  dull  muffled  tone.  In 
general  the  transition  is  quite  sharp  and  distinct.  This  is 
the  fourth  phase.  The  tone  gradually  or  quickly  ceases 
until  no  tone  is  heard.    This  is  the  fifth  phase  (Ettinger.) 

The  first  phase  is  due  to  the  sudden  expansion  of  the 
collapsed  portion  of  the  artery  below  the  cuff  and  to  the 
rapidity  of  the  blood  flow.  This  causes  the  first  sharp 
clicking  sound  which  measures  the  systolic  pressure. 

The  second,  or  murmur  and  sound  phase,  is  due  to  the 
whorls  in  the  blood  stream  as  the  pressure  is  further  re- 
leased and  the  part  of  the  artery  below  the  cuff  begins  to 
fill  with  blood. 

The  third  tone  phase  is  due  to  the  greater  expansion  of 
the  artery  and  to  the  lowered  velocity  in  the  artery.  A 
loud  tone  may  be  joroduced  by  a  stiff  artery  and  a  slow 
stream  or  by  an  elastic  artery  and  a  rapid  stream.  This 
tone  is  clear  cut  and  in  general  is  louder  than  the  first 
phase. 

The  fourth  phase  is  a  transition  from  the  third  and  be- 
comes duller  in  sound  as  the  artery  approaches  the  normal 
size. 

The  fifth  phase,  no  sound  i)liase,  occurs  when  the  pressure 
in  the  cuff  exerts  no  compression  on  the  artery  and  the 
vessel  is  full  throughout  its  length. 

It  is  generally  conceded  that  the  sounds  heard  are  pro- 
duced in  the  artery  itself  and  not  at  the  heart. 

The  tones  vary  greatly  in  different  hearts.  A  very 
strong  third  tone  phase  or  prolongation  of  this  phase  usu- 


92  AllTEKIOSCJ. Gliosis 

ally  nicaiis  that  the  heart  ^vhi('h  ])i'()(lu('es  the  tone  i.s  a 
.strongly  acting  one,  although  allowances  nmst  he  made  for 
a  sclei'osed  artery  in  wliich  there  is  a  tendency  to  the  pro- 
duction of  a  sharp  third  phase. 

AVeakness  of  the  third  phase,  as  a  rule,  indicates  weak- 
ness of  the  heart  and  this  dulling  of  the  thii'd  ])liase  may  be 
so  excessive  that  no  sound  is  ])ioduce(l.  (Joodman  and 
Howell  have  carried  this  method  further  l)y  measuring  the 
individual  phases  and  calculating  the  percentage  of  each 
phase  to  the  pulse  pressure.  Thus,  if  in  a  normal  individ- 
ual tlie  systolic  pressure  is  130  mm.,  the  diastolic  85  nun., 
and  the  pulse  pressure  45  mm.,  the  first  j)hase  lasts  from 
130  to  116  or  14  nnn.,  tlie  second  from  116  to  9G,  or  20  nun., 
the  third  from  96  to  91  or  5  nun.,  the  fourth  fi-om  91  to  85,  or 
6  nun.  The  lirst  phase  would  then  l)e  31.1  per  cent  of  the 
total  i^ulse  pressure,  the  second  ])hase  44.4  per  cent,  the 
third  phase  11.1  per  cent,  and  the  fourth  phase  13.3  i)er 
cent.  They  consider  that  the  second  and  third  phases  rep- 
resent cardiac  strength  (C.  S.)  and  the  first  and  fourth  rep- 
resent cardiac  weakness  (C.  AV.).  They  helieve  that  C.  S. 
should  normally  be  greater  than  C  \V.  In  the  example 
above  C.  S.  :C.  AV.^-  55.5:44.4.  In  weak  hearts,  especially  in 
uncompensated  hearts,  the  conditions  are  reversed  and  C. 
MV.  >  C.  S.  This  is  often  the  case.  As  a  heart  improves 
C.  S.  again  tends  to  become  greater  than  C.  AV.  They  think 
that  the  phases  should  be  studied  in  respect  to  the  sounds 
and  also  to  the  encroachment  of  one  sound  ui^on  another. 

These  ol)servations  are  interesting  l}ut  we  have  not  found 
the  division  into  phases  as  helijful  as  it  Avas  thought  to  be. 
AVe  spent  a  great  deal  of  time  on  this  question.  All  that 
can  l)e  said,  in  my  opinion,  is  that  a  loud,  long  third  phase 
is  usually  evidence  of  cardiac  strength. 

A  further  interesting  feature  which  can  be  heard  in  all 
irregular  hearts  is  a  great  difference  in  intensity  of  the  in- 
dividual sounds.  Cioodman  and  IFowell  call  this  i)henom- 
enon  tonal  arrhvthmia.    Irregularities  can  be  made  out  l)y 


PHYSIOLOGY    OF    THE    CIRCULATIOX  93 

tlie  aiiseiiltatory  inetliod  wliicli  can  not  be  lioai'd  at  tlie 
lieart. 

Ill  anemia  the  soniids  are  very  lond  and  clear  and  do  not 
seem  to  represent  the  actual  stren^'th  of  the  heart. 

The  general  lack  of  vasomotor  tone  in  the  blood  vessels 
together  with  some  atrophy  and  tiabbiiiess  of  the  coats 
probably  explains  the  lond  sounds. 

In  polycythemia  the  sounds  have  a  curious,  dull,  sticky 
character  and  can  not  be  differentiated  accurately  into 
phases,  a  condition  which  was  predicted  from  the  knowl- 
edge of  the  sliarj)  sounds  in  anemia. 

Ill  not  all  cases  can  all  i)hases  lie  made  out.  It  is  usually 
the  fourth  phase  which  fails  to  be  heard. 

In  such  cases  the  loud  third  tone  almost  immediately 
passes  to  the  (il'tli  ])hase  or  no  sound  [)hase.  The  importance 
of  this  will  later  be  taken  up. 

"Ill  arteriosclerosis,  with  hardening  and  loss  of  elasticity 
of  the  vessel  walls,  the  auscultatory  i)henoinena,  according 
to  Krylow,  are  apt  to  be  more  pronounced,  since  the  back 
pressure  at  the  cuff  probably  causes  some  dilatation  of  the 
vessel  above  it,  while  the  lumen  of  the  vessel  is  smaller 
than  normal.  Both  of  these  factors  cause  an  increased 
rapidity  in  the  transmission  of  the  l)l()od  wave  when  pres- 
sure in  the  cuff  is  released,  which  in  time  favors  the  vibra- 
tion of  the  vessel  walls. 

"In  high  grade  thickening  of  the  arterial  walls,  how- 
ever, especially  where  calcification  had  occurred,  Fischer 
found  that  the  sounds  were  distinctly  less  loud  ithan  nor- 
mal, the  more  so  in  the  arm,  which  showed  the  greater 
degree  of  hardening.  According  to  Ettinger's  exi^erience, 
the  rapidity  of  the  flow  distinctly  increases  the  auscultatory 
phenomenon."     (Gittings.) 

The  sounds  depend  upon  the  resonating  character  of  the 
cuff,  upon  the  size  and  accessibility  of  the  vessel,  npon  the 
force  of  the  heart  l)eat,  and  ui)on  the  velocity  of  the  l)lood. 


94 


ARTERIOSCLEROSIS 


The  Maximum  and  Minimum  Pressures 


The  maximum  (systolic)  pressure  is  read  at  the  point 
where  the  first  audible  click  is  heard  after  the  cuff  is  blown 
up  and  the  pressure  gradually  reduced  by  means  of  the 
needle  valve  in  the  hand  bulb  or  on  the  upright  of  the 
glass  containing  the  mercury.  All  are  agreed  upon  this 
l^oint.  There  has  been  some  dispute  as  to  the  place  where 
the  diastolic  pressure  should  be  read.  Korotkov  considered 
that  the  diastolic  pressure  should  be  read  at  the  fourth 


Fig.    29. — Tracing   of   auscultatory    phenomena.      (See    explanation    in    legend    of    Fig.    30.) 

phase  when  the  loud  tone  suddenly  becomes  dulled.  Others 
held  that  the  diastolic  pressure  should  be  read  at  the  fifth 
phase,  the  absence  of  all  sound.  Experiments  carried  out 
to  determine  tiiis  point  were  made  l)y  me  with  the  assist- 
ance of  Prof.  Kyster  and  Dr.  Meek  at  the  Physiological 
Laboratory  of  the  University  of  Wisconsin.  We  arranged 
apparatus  making  it  possible  to  hold  the  pressure  in  the 
carotid  arterv  of  dogs  at  maximum  or  minimum.    A  femoral 


PHYSIOLOGY    OF    THE    CIRCULATION  95 

arter}"  was  then  dissected  and  an  instrument  devised  to 
compress  the  -art<3ry  -with  a  water  jacket.  The  whole  was 
connected  up  with  a  kymograph.  A  time  marker  was  put 
in  so  as  to  record  the  place  wliere  changes  in  sound  w«re 
heard  while  listening  below  the  cuff  around  the  femoral 
artery.  Two  sets  of  records  were  taken.  One  with  pres- 
sure greater  than  minimum  pressure  and  a  falling  pres- 
sure over  the  femoral  artery  (Fig.  29),  tlie  other  with 
pressure  at  zero  and  gradually  raised  to  minimum  pres- 
sure (Fig.  30).    Both  sets  of  records  showed  the  same  re- 


Fig.  30. — Figures  are  to  be  read  from  left  to  right.  The  top  line  records  the  points 
where  sounds  were  heard,  the  figures  aoove  the  short  vertical  lines  refer  to  tones  (see 
text).  Mx.  1!.  P.,  maxinuini  blood-pressure.  M.  1>.  P.,  niininunn  blood-pressure.  P.  H., 
pressure  bulb"  recorder.  It  was  impossible  to  lower  and  raise  this  bulb  by  hand  without 
obtaining  the  great  irregular  oscillations  of  the  attached  lever  above  the  mercury  manom- 
eter.    B.   I..,  base  line. 

suit;  viz.,  that  at  a  point  corresponding  to  the  sudden 
change  of  tone  the  pressure  on  the  artery  corresponded  to 
the  minimum  pressure.  It  was  therefore  concluded  that 
experimentally  in  dogs  the  point  where  diastolic  pressure 
should  be  read  is  at  the  tone  change  from  clear  to  dull, 
not  at  the  point  where  all  sound  disappears. 

Erlanger  showed  some  years  ago,  that  with  his  instru- 
ment, the  point  at  which  diastolic  pressure  should  be  read 
was  at  the  instant  when  the  maximum  oscillation  of  the 


m 


ARTEIUOSCLEROHIS 


lever  suddenly  became  smaller.  While  checking*  up  the 
graphic  with  the  auscultatory  method  using  Erlanger's  in- 
strument, it  was  noticed  that  the  disapj3earance  of  all  sound 
did  not  correspond  with  the  sudden  diminution  of  the  os- 
cillation of  the  lever  connected  with  the  brachial  artery.  A 
series  of  records  were  carefully  made  on  patients.  It  was 
seen  that  during  the  period  of  the  third  tone  phase  the  os- 


Fig.    31. — Fast    driiin.      Sudden    dcrrease   in    size   of   ]iulse   wave   at    4,    marking   the   change 
from    clear    sharp    tone    to    dull    tone. 


ir^'"^     //^ 


^l      >V  W>^ 


\A/'H,my^ 


io-i2-i^ 


Vig.   32. — Slow   drum.      Sudden   decrease   in   amplitude   at   4. 

cillations  of  the  lever  on  the  drum  reached  a  maximum 
(Fig.  31)  and  remained  at  approximately  the  same  height 
for  some  millimeters  while  the  pressure  was  gradually  fall- 
ing. At  a  point  at  which  the  third  tone,  clear  and  distinct, 
became  dull,  there  was  an  appreciable  decrease  in  the  height 
of  the  pulse  wave.  P^rom  this  point  to  the  disappearance 
of  all  sound  there  was  a  gradual  diminution  of  the  size  of 
the  pulse  waves. 


PHYSIOLOGY    OF    THE    CIRCITLATION  97 

For  normal  pressures  the  difference  between  the  fourth 
(dull)  tone  and  the  fifth  (disappearance  of  all  tone)  phase, 
amounted  to  4  to  10  mm.  Occasionally  the  difference  was 
so  little,  the  change  from  sharp  third  tone  through  fourth 
dull  tone  to  disappearance  of  all  sound  was  so  abrupt,  that 
one  could  take  the  disappearance  of  all  sound  as  the  dias- 
tolic pressure,  with  an  error  of  not  more  than  2  to  4  mm. 
This  is  within  the  limits  of  normal  error  and  practically 
may  be  used  by  those  who  have  difficulty  in  noting  the 
change  from  third  to  fourth  phase.  For  high  pressures, 
however,  the  difference  between  fourth  and  fifth  phases  was 
never  less  than  8  mm.,  and  was  found  as  much  as  16  mm. 
The  diastolic,  therefore,  should  always  be  taken  at  the 
fourth  phase  if  possible. 

It  was  found  that  with  the  dial  instrument  the  greatest 
fling  of  the  lever  corresponded  to  the  third  phase  and  the 
sudden  lessened  amplitude  of  the  oscillation  was  at  the 
fourth  phase  and  was  coincident  with  the  change  of  tone 
from  sharp  to  dull.  Thus  the  diastolic  pressure  may  be 
read  off  on  the  dial  scale  by  watching  the  fling  of  the  hand 
and  with  some  practice  one  might  acquire  considerable  ac- 
curacy. It  is  better,  simpler,  and,  for  most  observers,  more 
accurate  to  use  the  stethoscope  and  hear  the  change  of 
sound. 

The  Relative  Importance  of  the  Systolic  and  Diastolic 

Pressures 

The  systolic  pressure  represents  the  maximum  force  of 
the  heart.  It  is  measured  by  noting  the  first  sound  audible 
over  the  brachial  artery  using  the  auscultatory  method. 
It  is  the  summation  of  two  factors  largely;  the  force  ex- 
pended in  opening  the  aortic  valves  (potential)  and  the 
force  expended  from  that  point  to  the  end  of  systole,  the 
force  w^hich  is  actually  driving  the  blood  to  the  periphery 
(kinetic).  To  start  the  blood  in  motion,  the  heart  must 
overcome  a  dead  weight  equal  to  the  sum  of  all  the  forces 


98  ARTERIOSCLEROSIS 

holding  the  aortic  valves  closed.  This  sum  of  factors, 
called  the  peripheral  resistance,  must  be  reached  and  passed 
by  the  force  of  the  ventricular  beat  before  one  drop  of 
blood  is  set  in  motion  along  the  aorta.  This  factor  of  re- 
sistance assumes  a  great  importance. 

The  systolic  pressure  is  always  fluctuating  as  it  depends 
upon  so  many  conditions,  and  the  calls  of  the  body  except 
during  sleep  are  many  and  various.  In  a  study  of  diurnal 
variations  in  arterial  blood  pressure  it  has  been  found  that — 
(1)  A  rise  of  maximum  pressure  averaging  8  mm.  of  Hg. 
occurs  immediately  on  the  ingestion  of  food.  A  gradual 
fall  then  takes  place  until  the  beginning  of  the  next  meal. 
There  is  also  a  slight  general  rise  of  the  maximum  pressure 
during  the  day.  (2)  The  range  of  maximum  pressure 
varies  considerably  in  different  individuals,  but  the  highest 
and  lowest  maximum  pressures  are  practically  equidistant 
from  the  average  pressure  of  any  one  individual.* 

The  pressure  is  lowest  during  sleep  and  gradually  rises 
near  the  end  of  sleep,  so  that  on  awakening  the  pressure 
was  the  same  as  before  sleep. 

Physiologically  there  are  many  conditions  which  modify 
the  systolic  pressure.  Sleep,  position,  meals,  exercise,  emo- 
tional states  cause  often  wdde  fluctuations  which  may  be 
very  sudden.  It  should  be  constantly  borne  in  mind,  that 
the  systolic  pressure  reading  which  is  made,  is  the  maxi- 
mum effort  of  the  heart  at  that  moment  only. 

The  diastolic  pressure  measures  the  peripheral  resistance. 
It  measures  the  work  of  the  heart,  the  potential  energy,  up 
to  the  moment  of  the  opening  of  the  aortic  valves.  It  is 
the  actual  pressure  in  the  aorta.  The  diastolic  pressure  is 
not  very  variable;  it  is  not  subject  to  the  same  influences 
which  disturb  the  systolic  pressure.  It  fluctuates  as  a  rule, 
within  a  small  range.  It  is  not  affected  by  diet,  by  mental 
excitement,  by  subconscious  psychic  influences,  to  anything 
like  the  extent  to  which  the  systolic  pressure  is  affected  by 


Weyse,    A.    W.,    and    Liitz.    V>.    R.:    Diurnal    X'ariations    in    Arterial    lilood    IMessurc, 
Am.  Jour.   I'hysiol.,  1915,  xxxvii,  330. 


PIIYSIOLOOV    OF    TIfE    CIIUTLATIOX  99 

the  action  of  these  factors.  The  diastolic  pressure  is  de- 
termined by  the  tone  in  the  arterioles  and  is  under  the  con- 
trol of  the  vasomotor  sympathetic  system.  Any  agent 
which  causes  chronic  irritation  of  the  whole  vasomotor  sys- 
tem produces  increase  in  the  peripheral  resistance  w^th  con- 
sequent rise  in  the  diastolic  pressure.  Any  agent  which 
acts  to  produce  thickening  of  the  walls  of  the  arterioles, 
narrowing  their  lumina,  produces  the  same  effect. 

Such  states  naturally  result  in  increased  work  on  the 
part  of  the  heart,  which  as  a  result,  hypertrophies  in  the 
left  ventricle.  The  increase  in  size  and  strength  is  a  com- 
pensatory process  in  order  to  keep  the  tissues  supplied 
with  their  requisite  quota  of  blood.  Conversely,  paralysis 
of  the  vasomotor  system  produces  fall  of  diastolic  pressure 
which,  if  long  contiimed,  results  in  death. 

The  diastolic  pressure  then  is  of  importance  for  the  fol- 
lowing reasons: 

1.  It  measures  peripheral  resistance. 

2.  It  is  the  measure  of  the  tonus  of  the  vasomotor  system. 

3.  It  is  one  of  the  points  to  determine  pulse  pressure. 

4.  Pulse  pressure  measures  the  actual  driving  force,  the 
kinetic  energy  of  the  heart. 

5.  It  enables  us  to  judge  of  the  volume  output,  for  pulse 
])ressure  which  is  only  determined  by  measuring  l)otli  sys- 
tolic and  diastolic  pressure,  is  such  an  index. 

6.  It  is  more  stable  than  the  systolic  pressure,  subject  to 
fewer  more  or  less  unknown  inlkiences. 

7.  It  is  increased  by  exercise. 

8.  It  is  increased  by  conditions  which  increase  periph- 
eral resistance. 

9.  The  gradual  increase  of  diastolic  pressure  means 
harder  work  for  the  heart  to  supply  the  parts  of  the  body 
with  blood. 

10.  Increased  diastolic  pressure  is  always  accompanied 
by  increased  pulse  pressure,  and  increased  size  of  the  left 
ventricle,  temporarily   (exercise)   or  permanently. 


1 00  AirPElUOSCLEROSrS 

11.  Decreased  diastolic  pressure  j>oes  liaud  in  hand  witli 
vasomotor  relaxation,  as  in  fevers,  etc. 

12.  Low  diastolic  pressure  is  frecpiently  ])atliog'nonionic 
of  aortic  insufficiency. 

13.  AVlien  the  systolic  and  diastolic  pressures  approach, 
heart  failure  is  inmiinent  either  when  pressure  picture  is 
high  or  low. 

When  all  these  factors  are  taken  into  consideration,  it 
becomes  apparent  that  the  diastolic  pressure  is  most  im- 
portant, if  not  the  most  important  part  of  the  pressure 
picture. 

Up  to  within  a  very  hrief  time  all  the  statistical  evidence 
of  blood  pressure  was  based  on  systolic  readings  alone. 
This  data  is  most  valuable  and  much  has  been  learned  as 
to  diagnosis  and  prognosis,  but  it  is  a  mass  of  data  based 
on  a  one-sided  picture  and  can  not  be  as  valuable  as  the 
statistics  which  will  undoubtedly  be  published  later  when 
all  the  pressure  picture  figures  can  be  analyzed. 

Pulse  Pressure 

The  pulse  pressure  is  the  actual  head  of  pressure  which 
is  forcing  the  blood  to  the  periphery.  At  every  systole  a 
certain  amount  of  blood  75-90  c.c.  (Howell)  is  thrown  vio- 
lently into  an  already  comfortably  filled  aorta.  The  sud- 
den ejection  of  this  blood  instigates  a  wave  which  rapidly 
passes  down  the  arteries  as  the  pulse  wave.  The  elastic 
recoil  of  the  aorta  and  large  arteries  near  the  heart  con- 
tract upon  the  blood  and  keep  it  moving  during  diastole. 
Normally  the  blood-vessels  are  highly  elastic  tubes  with 
an  almost  perfect  coefficient  of  elasticity.  The  pulse  pres- 
sure varies  under  normal  conditions  from  30  to  50  mm.  Hg. 
There  is  a  very  definite  relationship  between  the  velocity 
of  blood  and  the  pulse  pressure  which  is  expressed  thus; 
velocity  =  pulse  rate  x  pulse  pressure.* 


*Erlanger    and    Hooker:     An    Experimental    Study    of    I?Iood    Pressure    and    of    Pulse 
Pressure   in   Man,   Johns   Hoijkins   IIosp.    Kep.,    190-t,   xii,    145. 


PHYSIOLOGY    OF    THE    CHICULATIOX  101 

Further  it  has  been  demonstrated  that  under  normal  con- 
ditions and  during  various  procedures — ^tlie  pulse  pressure 
is  a  reliable  index  of  the  systolic  outi)ut.* 

Increased  pulse  pressure  therefore  goes  hand  in  hand 
with  greater  systolic  output.  Physiologically  this  is  most 
ideally  seen  during  exercise.  Following  exercise  the  pulse 
rate  increases,  the  systolic  pressure  rises  greatly,  the  dias- 
tolic slightly  or  not  at  all.  The  pulse  pressure  therefore  is 
increased.  The  velocity  also  is  nmch  increased.  The  call 
comes  for  more  blood  and  the  heart  responds.  In  the  chronic 
high  pulse  pressures  there  are  four  correlated  conditions 
which,  so  far  as  I  have  studied  them,  are  always  present. 
These  are:  (1)  An  increase  in  size  of  the  cavity  of  the  left 
ventricle.  The  ventricle  actually  by  measurement  contains 
more  blood  than  normal,  and  therefore  throws  out  more 
blood  at  every  systole.  The  volume  output  is  greater  per 
unit  of  time.  (2)  There  is  actual  permanent  increase  in 
diameter  of  the  arch  of  the  aorta.  This  is  a  compensating 
process  to  accommodate  the  increased  charge  from  the  left 
ventricle,  (3)  There  are  on  careful  auscultation  over  the 
manubrium,  joarticularly  the  lower  half,  breath  sounds 
which  vary  from  bronchial  to  intensely  tubular,  depending 
upon  the  anatomic  placing  of  the  aorta,  the  shape  of  the 
chest,  and  the  degree  of  dilatation.  Often  there  is  very 
slight  impairment  of  the  percussion  note  as  well.  (4) 
There  is  increase  in  size  of  all  the  large  distributing  ar- 
teries, carotids,  brachials,  femorals,  renals,  celiac  axis,  etc., 
with  fibrous  changes  in  the  media,  loss  of  some  elasticity, 
and  increase  in  size  of  the  pulse  wave.  Increased  pulse 
pressure  means  increased  volume  outi)ut,  but  does  not  al- 
ways mean  increased  velocity.  The  proper  distribution  of 
blood  to  the  various  organs  of  the  body  is  regulated  by  the 
vasomotor  system  acting  upon  the  small  arteries  which  con- 
tain considerable  unstriated  nuiscle.  When  fibrous  ar- 
teriosclerosis is  present  there  is  loss  of  elasticity  in  the  dis- 

*Dawson    and    Gorhani:      The    Pulse    Pressure    as   an    Index    of    Systolic    Output,    lour 
Kxper.  Med.,  1908,  x,  484. 


102  AirrKIMOSCLKltOSIS 

ti'il)iitiiii>'  arteries  and  a  j^ivator  voluiiio  of  ])1()()(1  must  be 
thrown  out  l)y  the  ventricle  at  every  systole  in  order  that 
every  or^'an  shall  have  its  full  (^uota  of  blood.  A  force 
which  is  sufficient  to  send  blood  through  elastic  normal  dis- 
tributing- tul)es  l)ecomes  totally  insufficient  to  send  the  same 
amount  of  blood  through  tortuous  and  more  or  less  inelastic 
tubes. 

It  is  evident  then  that  pulse  pressure  is  exceedingly  im- 
portant. It  can  only  be  determined  by  measuring  both  the 
^ijsfolic  and  diastolic  pressure.  The  pulse  rat(^  nuist  also 
be  known  in  order  to  compute  the  velocity.  It  is  essential 
to  have  the  whole  pressure  picture  for  all  cases  if  correct 
conclusions  are  to  be  drawn. 

In  an  irregular  heart,  especially  in  the  cases  due  to  myo- 
cardial disease,  it  is  quite  impossible  to  determine  the  true 
diastolic  pressure.  One  can  only  approximate  it  and  say 
that  the  pulse  pressure  is  low^  or  high.  As  a  matter  of  fact 
the  real  systolic  pressure  can  not  be  determined.  For  this 
figure  the  place  on  the  scale  where  most  of  the  beats  are 
heard  may  be  taken  for  the  average  systolic  pressure.  No 
one  can  seriously  maintain  that  he  can  measure  the  dias- 
tolic pressure  under  all  circumstances. 

By  means  of  the  auscultatory  method  of  measuring  blood 
pressure  we  are  able  to  determine  irregularities  of  force  in 
the  heart  beats  more  easily  than  by  listening  to  the  heart 
sounds.  A  pulsus  alternans  is  i-eadily  made  out.  Tlie  ir- 
regular tones  heard  over  the  brachial  artery  in  cases  of  ir- 
regular heart  action  have  been  called  'Honal  arrhythmias." 

Blood  Pressure  Variations 

A  recent  study  of  diurnal  variations  in  blood  pressure  has 
shown  that  while  the  maximum  i)ressure  rises  after  the  in- 
gestion of  food  and  steadily  rises  slightly  througliout  the 
day,  the  minimum  ])l()od  ])ressure  is  very  uniform  through- 
out the  day,  and  is  little  affected  by  the  ingestion  and  di- 
gestion of  meals.    AVlien  it  is  affected,  a  rise  or  a  fall  mav 


PHVSIOLOCY    OF    TIIK    CIIlCrLATlOX  103 

take  place.    Tlirouglioiit  tlie  day,  it  tends  to  l)eeoiiie  sliglitly 
lower.    The  pulse  pressure  then  is  greater  towards  evening. 
AVeysse  and  Lutz  in  a  study  of  this  question  draw  the  fol- 
lowing conclusions: 

1.  A  rise  of  inaxiniuni  pressure  averaging  8  mm.  of  IFg 
occui's  immediately  on  the  ingestion  of  food.  A  gradual 
fall  then  takes  place  until  the  beginning  of  the  next  meal. 
There  is  also  a  slight  general  rise  of  the  maxinuim  pressure 
during  tlie  day. 

2.  The  average  maximum  hlood  ])ressure  for  healthy 
young  men  in  the  neigli))Oi-hood  of  20  years  of  age  is  120 
nun.  of  ]ig.  This  pressure  obtains  connnonly  one  hour 
after  meals.  The  higher  maxinuim  pressures  occur  imme- 
diately after  meals,  and  the  lower,  as  a  rule,  immediately 
before  meals. 

3.  The  range  of  maxinuun  pressure  varies  considerably  in 
different  individuals,  but  the  highest  and  lowest  nuixinuun. 
pressures  are  practically  equidistant  from  the  average  pres- 
sure of  any  one  individual. 

4.  The  mininuim  blood  pressure  is  very  uniform  through- 
out the  day,  and  is  little  affected  by  the  ingestion  and  diges- 
tion of  meals.  AVhen  it  is  atfected  a  rise  or  fall  may  take 
place.  There  is  a  tendency  for  a  slight  general  lowering 
of  the  mininmm  pressure  throughout  the  day. 

5.  The  average  minimum  blood  ])ressure  for  healthy 
young  men  in  the  neighborhood  of  20  years  of  age  is  85  nun. 
of  l^f^.  Thus  we  get  an  average  pulse  pi-essure  of  35  mm. 
oflTg. 

6.  Pulse  pi-essure,  pulse  rate,  and  the  I'elative  velocity 
of  the  blood  ilow  are  inci'eased  inunediately  ui)()n  the  inges- 
tion of  meals.  They  attain  the  maxinuun,  as  a  rule,  in 
half  an  hour,  and  then  decline  slowly  until  the  next  meal. 
There  is  a  general  increase  in  each  thi'oughout  the  day. 

These  measurements  were  made  u])on  pei'sons  at  rest. 
Almost  any  form  of  exercise  would  have  made  the  varia- 
tions much  greater.     Xo  account  is  taken  of  the  j)sychic 


104 


AIITEIUOSCLEROSIS 


Thk    Average 

Diurnal   Blood   Pressure 

Eecord 

op  the  Ten  Subjects 

TiMi; 

MAXI- 

MINI- 

MEAN 

pui.si; 

PRES- 

PUI.SB 

PP   X   PR 

NOTES 

MUM 

MUM 

SURE 

mm.  Ilg 

mm.  Hg 

mm-.  Hg 

Him.  Hg 

4:;50  p.m 

119.5 

84.1 

101.8 

35.4 

72.0 

2549 

5:00  p.m 

117.7 

83.5 

100.6 

34.2 

71.1 

2432 

fiiOO  p.m 

118.0 

84.0 

101.0 

34.0 

74.9 

2547 

Before  dinner 

0:45  p.m 

127.2 

88.2 

107.7 

39.0 

78.1 

3046 

After  dinner 

7:00  p.m 

124.7 

87.7 

106.2 

37.0 

76.0 

2*12 

7:30  p.m 

122.0 

83.4 

102.7 

38.6 

76.0 

2934 

8:00  p.m 

122.4 

85.5 

103.4 

36.9 

71.2 

2527 

8:30  p.m 

120.0 

85.0 

102.5 

35.0 

69.7 

2439 

9:00  p.m 

120.5 

84.7 

102.5 

35.8 

65.2 

2334 

9:30  p.m 

118.2 

84.4 

101.6 

33.8 

64.4 

2177 

7:30  a.m 

118.4 

87.6 

1D3.0 

30.8 

70.3 

2165 

8:00  a.iii 

116.4 

86.4 

101.4 

30.0 

69.8 

2094 

Before   breakfast 

8:30   a.m 

124.2 

85.4 

104.8 

38.8 

79.4 

3081 

After  breakfast 

9:00  a.m 

123.8 

84.4 

104.1 

39.4 

84.1 

3313 

10:00  a.m 

118.2 

83.6 

100.9 

34.6 

70.7 

2446 

11:00  a.m 

116.2 

84.8 

100.5 

31.4 

67.7 

2126 

12:00  m     

114.4 

83.2 

98.8 

31.2 

66.2 

2065 

Before  lunclieon 

12:30  p.m 

122.8 

83.2 

103.0 

39.6 

70.9 

2808 

After  luncheon 

1:00  p.m 

122.3 

82.0 

102.1 

40.3 

79.7 

3212 

2:00  p.m 

118.4 

81.4 

99.9 

37.0 

77.6 

2871 

3:00  p.m 

118.8 

82.6 

100.7 

36.2 

75.1 

2719 

4:00  p.m 

115.8 

82.0 

98.9 

33.8 

71.9 

2420 

5:00  p.m 

117.2 

83.4 

100.3 

33.8 

69.6 

2352 

6:00  p.m 

117.4 

84.4 

100.9 

33.0 

72.8 

2402 

Before  dinner 

6:45  p.m 

124.6 

83.1 

103.8 

41.5 

80.4 

3337 

After  dinner 

7:00  p.m 

125.2 

84.2 

104.7 

41.0 

76.1 

3120 

7:30  p.m 

122.0 

84.0 

103.0 

38.0 

73.7 

2801 

8:00  p.m 

119.6 

85.0 

102.3 

34.6 

72.3 

2502 

8:30  p.m 

119.7 

84.0 

101.3 

34.7 

69.0 

2394 

9:00  p.m 

120.0 

86.2 

103.1 

33.8 

68.0 

2298 

Average.  . 

120.0 

85.0 

102.5 

35.0 

72.0 

2550 

(Taken  from  Weysse  and  Lutz.) 


variations  whicli  for  the  physician  are  the  most  important 
to  bear  in  mind.  Neglect  to  take  this  variation  into  ac- 
count will  inevitably  lead  to  false  conclusions. 

In  some  experiments  to  determine  the  changes  upon  the 
blood  pressure  induced  by  hot  and  cold  applications  on  and 
within  the  abdomen,  Hammett,  Tice  and  Larson  found  that 
heat  applied  to  the  outside  of  the  abdomen  raises  the  blood 
pressure.  The  application  of  cold  produces  no  change.  Ei- 
ther hot  or  cold  saline  introduced  within  the  abdomen 
causes  a  fall  in  blood  pressure. 


PHYSIOLOGY    OF    THE    CIIICULATIOX  105 

Experimentally,  certain  drugs  such  as  adrenalin,  barium 
chloride,  nicotine,  digitalis,  strophanthus  and  the  infundib- 
ular portion  of  the  pituitary  body  known  as  pituitrin  raise 
the  maxinmm  pressure.  In  the  clinic  it  is  difficult  to  con- 
clude always  whether  the  drug  alone  is  responsible  for  rise 
in  maximum  pressure.  Adrenalin  given  intravenously  will 
raise  the  pressure.  So  will  digitalis  and  strophanthus.  I 
have  watched  the  maxinmm  pressure  rise  within  three  min- 
utes following  an  intravenous  injection  of  gr.  Moo  (0.0006 
gni.)  strophanthin  20  nnn.  of  lig;  I  have  seen  the  subcu- 
taneous injection  of  10  minims  of  adrenalin  repeated  sev- 
eral times  daily  for  six  months  fail  to  have  the  least  effect 
on  the  blood  pressure  picture. 

Elevation  of  the  foot  of  the  bed  about  nine  inches  proved 
so  efficacious  in  steadying  failing  hearts  in  acute  infectious 
diseases,  particularly  typhoid,  that  a  study  was  made  of 
the  effect  upon  blood  pressure.  Many  observations  were 
made,  but  no  instrumental  proof  of  rise  in  blood  pressure 
could  be  adduced. 

Exercise  always  raises  blood  pi'essure,  the  maximum 
much  more  than  the  mininmm.  In  athletes  the  minimum 
pressure  may  actually  fall,  the  maxinmm  rise  so  that  a 
greater  volume  output  results  from  the  greater  juilse  pres- 
sure. 

Shock  and  hemorrhage  lower  it.  llemori'liage  lowers 
also  the  pulse  pressure,  and  it  may  ])e  jwssible  to  prognos- 
ticate internal  hemorrhage  by  frequent  estimations  of  the 
systolic  and  diastolic  pressui'es  (AViggers).  Compression 
of  the  superior  mesenteiic  artery  or  the  celiac  axis  in  dogs 
raises  the  blood  pressure  measured  in  the  carotid  artery 
for  a  i^eriod  of  at  least  an  hour.  This  seems  to  l)e  depend- 
ent on  purely  mechanical  causes,  and  is  not  a  reflex  vaso- 
motor phenomenon.    (Longcope  and  iMcClintock.) 

Experimentally  blood  pressure  can  be  increased  by  di- 
rect compression  of  tlie  bi'ain  as  Cushing  has  shown.  It  was 
thought  at  one  time  that  in  man  the  same  effect  would  re- 


lOG  ARTKIllOSC'LlillOSIS 

suit  i'roiu  tiiinor  of  the  l)raiii  or  osi)('('ially  froiii  subdural 
or  extradural  liouiorrlia^e  following  head  injuries.  This, 
however,  is  not  the  case.  No  information  of  great  value 
can  be  ol)tained  by  the  measurement  of  l)lood  pressure  in 
these  states.  AYe  do  know  that  too  high  and  too  prolonged 
compression  of  the  medulla  brings  about  exhaustion  of  the 
cardiac  center  accompanied  with  rapid  pulse,  low  pressure 
and  eventual  death. 

Hypertension 

All  the  conflict  during  the  past  few  years  over  the  sub- 
ject of  blood  pressure  has  revolved  around  this  much  over- 
Avorked  word.  Hypertension  means  high  pressure,  and  yet 
it  carries  with  it  a  suggestion  of  high  pressure  which  is 
harmful  to  the  individual.  As  a  matter  of  fact  hyperten- 
sion is  a  compensatory  process,  it  is  often  a  saving  process 
in  sjoite  of  the  fact  that  it  carries  i^ossibilities  of  harm  in 
its  possessor.  It  has  been  made  a  fetish,  a  god  to  fall  down 
before  and  worship  and  it  has  been  the  means  of  holding  a 
torch  of  fear  over  a  patient  which  has  not  been  lost  on  the 
charlatans.  Popularization  of  blood  pressure  has  brought 
its  crojD  of  evils,  no  one  of  which  has  been  as  fruitful  in 
dollars  to  unprincipled  quacks  as  hypertension. 

Hypertension  is  the  expression  on  the  part  of  the  circu- 
lation to  meet  new  conditions  in  the  tissues  so  that  all  tis- 
sues will  bo  nourished  and  all  will  l)e  enabled  to  function. 
Looked  at  from  that  point  of  view  it  is  a  conservative  proc- 
ess and  in  many  cases  it  is.  It  is  not  an  average  normal 
state,  but  it  is  normal  state  for  the  man  who  has  it  in 
clironic  form.  Hypertension  should  l)e  viewed  rationally 
and  its  proper  j)lace  in  the  whole  make-up  of  the  patient  de- 
termined. Hypertension  is  a  relative  term.  AVhat  might 
be  high  pressure  in  a  man  of  sedentary  habits  who  reaches 
the  age  of  fifty,  might  not  l)e  high  jn-essure  in  a  full  blooded 
formerly  athletic  man  of  the  same  age.  Temi)orary  hyper- 
tension due  to  excitement,  exercise,  etc.,  must  be  kept  in 


THYSIOLOGY    OF    THE    CIKCULATIOX  107 

mind.  It  is  not  intended  to  convey  the  impression  tliat 
hypertension  is  of  no  moment.  It  is  a  matter  for  investi- 
gation, hnt  not  a  matter  to  worship  as  the  all-in-all. 

Hypertension  is,  after  all,  a  physiologic  response  on  the 
part  of  the  organism  in  order  to  maintain  the  circulation  in 
equilibrium  in  the  face  of  conditions  which  tend  to  produce 
vasoconstriction  in  large  areas  and,  therefore  tend  to  de- 
prive these  areas  of  blood.  That  there  nmst  be  some  sub- 
stance in  the  ])lood  stream  which  causes  this  constriction 
seems  certain.  What  it  is,  is  not  at  present  known.  Re- 
cently, Voegtlin  and  Macht*  have  isolated  a  crystalline  sub- 
stance from  the  blood  of  man  and  other  mannnals  which 
they  regard  as  a  lipoid  and  closely  related  to  cholesterin. 
This  substance  was  recovered  by  them  from  the  cortex  of 
the  adrenal  gland.  This  becomes  of  added  interest  in  the 
light  of  observations  made  by  Gubar  (quoted  by  Voegtlin 
and  Macht).  He  noted  "that  the  vasoconstricting  proper- 
ties of  blood  serum  vary  in  ditferent  pathologic  conditions, 
being  increased  in  nephritis,  for  instance,  and  diminished 
in  others."  In  some  experiments  made  in  the  sunnner  of 
1913,  we  found  there  was  no  marked  difference  in  the  ana- 
phylactic shock  produced  in  lialf-grown  rabbits  by  the  in- 
jection of  normal  and  uremic  blood  serum.  As  lipoids  do 
not  cause  anaphylaxis,  there  should  be  no  difference  in  the 
reaction  of  normal  and  uremic  sera  unless  in  one  tliere  was 
some  form  of  protein  not  in  the  other.  This  does  not  seem 
to  be  the  case.  The  presence  of  something  in  the  circula- 
tion, therefore,  produces  constriction  of  vessels.  This  calls 
for  more  force  in  contraction  on  the  part  of  the  heart.  This 
substance  may  be  of  lipoid  nature.  The  continued  presence 
of  this  hypothetical  substance  naturally  would  lead  to  hy- 
j)ertrophy  of  the  heart. 

AVhat  makes  hypei'tension  of  significance  is  not  the  hy- 
pertension itself,  l)ut  the  fact  that  it  is  the  exjnvssion  of 

•Isolation  of  a  Xew  \'asoconstrictor  Sul)staiicc  from  the  lilood  ami  the  Adrenal  Cor- 
tex, Jour.  Ani.   Med.  Assn.,  1913,  Ixi,  2136. 


108  ARTEIMOSCLEROSIS 

processes  going  on  in  tiie  body  wliicli  demand  exliaustive 
investigation.  To  attacli  a  blood  pressure  cuff  to  tlie  arm, 
find  tlie  pressure,  and  diagnose  liypertension  is  like  putting 
a  thermometer  under  the  tongue,  noting  a  rise  in  the  mer- 
cury, and  diagnosing  fever.  What  causes  the  liyperten- 
sion? Can  the  causes  be  removed!  Those  are  the  really 
vital  questions  after  the  symptom  hypertension  has  been 
discovered. 

All  states  of  hypertension  are  accompanied  by  more  or 
less  increase  of  pulse  pressure.  In  other  words  the  systolic 
pressure  is  always  increased  to  greater  degree  than  the  di- 
astolic pressure.  In  studies  carried  out  in  the  wards  and 
Pathological  Laboratory  of  the  Milwaukee  County  Hospi- 
tal, Milwaukee,  we  found  that  in  all  of  the  cases  of  chronic 
high  blood  pressure  with  resulting  high  pulse  pressure  four 
correlated  factors  were  found.  If  any  one  of  these  factors 
is  present,  the  other  three  are  found. 

1.  In  all  high  pulse  pressure  cases  there  is  increase  in  the 
size  of  the  cavity  of  the  left  ventricle.  The  ventricle  actu- 
ally contains  more  blood  Avhen  it  is  full,  and  throws  out, 
therefore,  more  blood  at  each  systole.  The  actual  volume 
output  is  greater  per  unit  of  time.  Such  hearts  always 
show  increase  in  thickness  of  the  ventricular  wall.  I  quite 
agree  with  Stone,*  who  says,  "It  is  merely  to  be  empha- 
sized that  when  the  pulse  pressure  persistently  equals  the 
diastolic  pressure  (high  pressure  pulse,  in  other  words) 
with  a  resulting  50  per  cent,  overload,  which  means  the  ex- 
penditure of  double  the  normal  amount  of  kinetic  energy  on 
the  part  of  the  heart  inuscle,  cardiac  hypertrophy  has  oc- 
curred." They  are  found  in  aortic  insufficiency,  in  chronic 
nephritis,  in  the  diffuse  fibrous  type  of  arteriosclerosis,  and 
in  some  cases  of  exophthalmic  goiter.  Such  a  condition 
occurs  temporarily  after  exercise. 


*Stone,   W.   J.:      The   Differentiation   of   Cerebral   and   Cardiac   Types    of   Hyperarterial 
Tension  in  Vascular  Diseases,  Arch.  Int.  Med.,  November,   1915,  p.   775. 


PHYSIOLOGY    OF    THE    CIRCULATION  109 

2.  In  all  high  pulse  pressure  cases  there  is  actual  per- 
manent increase  in  diameter  of  the  arch  of  the  aorta.  This 
is  a  compensating  process  to  accommodate  the  increased 
charge  from  the  left  ventricle.  Smith  and  Kilgore*  have 
shown  this  to  be  true  in  cases  of  chronic  nephritis  with  hy- 
pertension. Their  research  confirms  my  own  observations. 
They  found  dilatation  of  the  arch  in  (1)  syphilis  (that  is, 
aortitis);  (2)  age  over  50  (that  is,  probable  factor  of  ar- 
teriosclerosis); (3)  other  serious  cardiac  enlargement,  and 
(4)  hypertension  (with  more  or  less  hypertrophy,  as  in 
chronic  nephritis). 

In  ten  cases  showing  arches  at  the  upper  limit  of  normal 
(that  is,  6  cm.  in  diameter)  and  hypertrophy  of  the  heart, 
three  were  chronic  mitral  endocarditis;  one  was  chronic 
aortic  endocarditis;  three  were  chronic  mitral  and  aortic 
endocarditis,  and  there  was  one  each  of  hyperthyroidism, 
pericarditis  and  adherent  pericardium. 

In  fourteen  cases  of  hypertension  (highest  systolic  270 
mm.,  average  systolic,  215  mm.),  all  showed  cardiac  hy- 
pertrophy. ''All  but  three  of  these  cases  had  great  ves- 
sels whose  transverse  diameters  measured  over  the  normal 
limit  of  6  cm.,  and  in  one  of  those  measuring  6  cm.  the 
Roentgen-ray  diagnosis  was  'slight  dilatation'  of  the 
arch."  Smith  and  Kilgore  are  at  a  loss  to  explain  the  three 
exceptions.  They  did  not  give  diastolic  pressures,  so  pulse 
pressures  are  not  known.  Possibly  the  three  exceptions 
were  cases  of  high  diastolic  pressure  in  which  the  pulse 
pressure  possible  was  not  over  60  mm.  Such  cases  might 
show  "slight  dilatation  of  the  arch,"  but  not  marked  dila- 
tation, such  as  was  found  in  the  other,  evidently  high  pulse 
pressure  cases. 

We  have  found  that  only  the  high  pulse  pressure  cases 
show  dilatation  of  the  arch.  Certain  high  tension  cases 
which  have  had  a  very  high  diastolic  pressure  do  not  re- 
veal anv  accuratelv  measurable  dilatation  of  the   aortic 


*Smith,   W.   TI.,  and  Kilgore,  A.   R. :     Dilatation  of  the  Arch   of  the  Aorta   in   Chronic 
Nephritis  with   Hypertension,  Am.  Jour.    ^led.    Sc,   1915,  cxlix,   503. 


110  ArvTElllOSCLEROSlrt 

arch.  An  onii)ly  aorta  after  death  is  quite  different  from  a 
fnnctionatiiig'  aorta  during  life.  Hence  the  dihitation 
which  is  found  postmortem  must  have  been  considerable 
during  life.  And  conversely,  a  dilatation  which  was  pres- 
ent during  life  might  not  be  looked  on  as  such  after  death. 

3.  Tn  all  high  i)ulse  pressure  cases  one  will  tind  on  care- 
ful auscultation  over  the  manubrium,  particularly  its  lower 
half,  breath  sounds  which  vary  from  bronchial  to  intensely 
tubular.  At  times  the  percussion  note  will  be  slightly  im- 
paired, as  McCrae*  has  shown  in  dilatation  of  the  arch  of 
the  aorta.  This  auscultatory  sign  is  evidence  of  some  more 
or  less  solid  body  in  the  anterior  mediastinum  which  is 
lying  on  the  trachea  and  permits  the  normal  tubular  breath- 
ing in  the  trachea  to  be  audible  over  the  upper  part  of  the 
sternum.  It  is  found  in  cases  of  dilated  aortic  arch.  Flu- 
oroscopic examination  has  confirmed  the  findings  on  auscul- 
tation. 

4.  In  all  high  pulse  pressure  cases,  in  which  the  jiulse 
pressure  is  over  70  mm.  of  mercury,  there  is  increase  in 
the  size  of  all  large  distributing  arteries,  carotids,  brachials, 
femorals,  renals,  celiac  axis,  etc.,  with  fibrous  changes  in 
the  media,  loss  of  some  of  the  elasticity,  and  in  the  palpable 
superficial  arteries,  increase  in  size  of  the  pulse  wave. 

Increased  pulse  pressure  means  increased  volume  output, 
but  does  not  always  mean  increased  velocity.  The  proper 
distribution  of  blood  to  the  various  organs  of  the  body  is 
regulated  by  the  vasomotor  system  acting  on  the  small  ar- 
teries wdiich  contain  considerable  unstriated  muscle.  In 
order  that  there  may  be  enough  blood  at  all  times  and  under 
varying  conditions  of  rest  and  function,  there  must  be  a 
proper  supply  coming  through  the  distributing  vessels,  the 
large  arteries,  those  containing  much  elastic  tissue,  and 
only  a  very  small  amount  of  unstriated  muscle  tissue  or 
none  whatever.  Fibrous  sclerosis  of  these  vessels  causes 
them  to  become  enlarged  and  tortuous  and  to  lose  much 


*\rcCrac.    Tlionias:      Dilatation    of   the    Arch   of   the   Aorta,    Am.    Tour.    Mod.    Sc,    1910, 
cxl,   469. 


PHYSIOLOGY    OF    THE    (MRCTI.ATIOX  111 

of  their  elasticity,  which  is  essential  for  the  even  distribu- 
tion of  blood.  A  g-reater  blood  volume  is  therefore  neces- 
sary in  order  that  the  organs  may  receive  their  quota  of 
blood.  A  force  which  is  sufficient  to  send  blood  through 
elastic  normal  distributing  tubes  becomes  totally  insufficient 
to  send  the  same  amount  of  blood  through  tortuous  and 
more  or  less  inelastic  tubes.  As  a  compensatory  process 
the  pulse  pressure  increases.  For  this  to  increase,  the  left 
ventricular  cavity  dilates,  the  arch  dilates,  and  as  a  greater 
force  must  be  exerted  to  keep  the  increased  mass  in  motion, 
the  heart  responds  by  hypertrophy  of  its  left  ventricle  and 
becomes  itself  the  subject  of  fibrous  changes  in  the  myo- 
cardium. The  mass  movement  of  blood  is  therefore  greater 
in  high  pulse  pressure  cases  than  in  cases  of  normal  pulse 
pressure. 

In  cases  of  chronic  interstitial  nephritis — contracted 
granular  kidney — it  may  well  be  that  the  sclerosis  of  the 
arteries  is  a  secondary  process  caused,  as  Adami  thinks, 
by  the  hypertension  itself.  In  aortic  insufficiency  the  situ- 
ation is  somewhat  different.  The  high  pulse  ])ressure  is  due 
to  a  very  low  diastolic  pressure,  for  in  my  experience  with 
uncomplicated  aortic  insufficiency  the  systolic  pressure  is, 
as  a  rule,  not  much  increased  above  the  normal  for  the  in- 
dividual's age.  Here  peripheral  resistance  is  so  low  that 
a  capillary  ])ulse  is  common.  The  volume  output  per  unit 
of  time  is  greatly  increased,  the  arch  of  the  aorta  is  dilated, 
and  the  i)ulse  is  large.  The  fact  that  a  large  part  of  the 
blood  regurgitates  during  diastole  back  into  the  ventricle, 
and  the  fact  that  the  diastolic  pressure  is  low  means  that 
there  is  no  increased  resistance  to  overcome,  and  the  sys- 
tolic pressure  is  not  raised. 

Stone*  has  divided  the  cases  of  hypertension  into  the  cere- 
bral and  cardiac  types.  He  finds  that  there  is  a  difference 
in  prognosis  and  in  the  mode  of  death  in  the  two  groups. 
He  has  further  attem])ted  to  judge  of  the  work  i)laced  upon 

*Stone,  \V.  J.:     Arch.   Int.   Med.,   1915,   xvl,   r7.S. 


]]2  ARTERIOSCLEROSIS 

tlio  licai-t  l)y  ('al('ulatiii,i>'  Avliat  Ik^  calls  the  heart  load  or  pres- 
sui'c-i-atio.  For  example,  he  takes  a  normal  pressure  at 
]20-8()-4().  The  relation  between  80  and  40  is  Vs  or  50  per 
cent.  That  he  considers  normal.  When  the  heart  load  in- 
creases so  that  the  pulse  jiressure  equals  or  exceeds  the 
diastolic  pressure,  the  heart  load  is  TOO  per  cent  or  more, 
he  considers  the  danger  of  myocardial  exhaustion  graver 
than  when  the  heart  load  is  normal  or  less  than  50  per  cent. 

It  is  his  opinion,  in  which  I  heartily  concur,  'Hhat  an 
individual  with  a  systolic  pressure  of  200  and  a  diastolic 
pressure  of  140,  is  in  greater  danger  of  cerebral  death  than 
an  individual  with  a  systolic  pressure  of  200  and  a  diastolic 
pressure  of  100."  He  is  ''likewise  certain  that  the  indi- 
vidual with  a  systolic  pressure  of  200  and  a  diastolic  of 
90  to  100  is  in  greater  danger  of  a  cardiac  death.  It  is 
apparently  the  constant  high  diastolic  pressure  rather  than 
the  intermittently  high  systolic  pressure  which  predisposes 
to  cerebral  accident." 

I  have  not  been  able  to  confirm  all  of  Stone 's  conclusions. 
His  contention  holds  good  for  some  cases,  but  not,  in  my 
experience,  for  the  great  majority  of  the  hypertension  cases. 
I  feel  that  in  the  classification  of  the  chronic  high  pressure 
case  we  can  go  one  step  farther  and  split  his  first  group 
into  two  usually  differentiable  groups.  Syphilis  is  not  an 
etiological  factor  in  any  of  these  groups.  It  is  not  consid- 
ered that  these  groups  are  absolutely  distinct  and  can  al- 
ways be  rigidly  separated.  There  are  variations  and  com- 
binations which  render  an  exact  separation  impossible. 
But  bearing  this  in  mind  the  following  classification  is  pro- 
posed as  a  working  classification. 

Group  A.  Chronic  nephritis. 

Group  B.  Essential  hypertension. 

Group  C.  Arteriosclerotic  hypertension. 

Group  A.  Chronic  NepliriUs.  These  are  the  cases  with 
a  high-pressure  picture,  that  is  to  say,  high  systolic  (200+) 
and  high  diastolic  (120-140 +).    The  pulse  pressure  is  much 


PirYSIOLOCV    OF    TirE    CITUTLATIOX  111] 

increased.  The  palpable  arteries  are  hard  and  fibrous. 
There  is  puffiness  of  the  under  eyelids,  which  is  more  pro- 
nounced in  the  morning  on  arising.  Polyuria  with  low 
specific  gravity  and  nycturia  are  present.  There  are  almost 
constant  traces  of  albumin  in  the  urine,  with  hyaline  and 
finely  granular  casts. 

Functionally  these  kidneys  are  much  under  normal.  The 
functional  capacity  determined  l)y  Mosenthal's  modification 
of  the  Schlayer-Hedinger  method  shows  a  marked  inability 
to  concentrate^  salts  and  nitrogen,  Tlie  phtlialein  output 
is  l)el()w  normal.  As  the  case  advances  the  phthalcin  out])ut 
becomes  less  and  less,  until  a  period  is  readied  wlien  tliere 
ar(^  only  traces  or  c()m))lete  sui)pression  at  tlic  end  of  a  two- 
liour  period.  Sucli  ])atients  may  live  for  ten  weeks  (one  of 
our  cases)  or  longer,  all  the  time  sliowing  mild  uremic 
symptoms,  and  suddenly  pass  into  coma  and  die. 

The  natural  end  of  patients  in  this  group  is  either  uremia 
or  cardiac  decompensation  (so-called  cardiorenal  disease). 
Cerebral  accidents  may  happen  to  a  small  number.  It  is 
only  to  tliis  group,  in  my  opinion,  tliat  th(^  term  cardiorenal 
disease  should  be  applied.  Formerly  I  believed  that  all  high 
systolic  j3ressure  cases  were  cases  of  chronic  nephritis  of 
some  definite  degree.  From  the  purely  pathologic  stand- 
point that  is  true,  but  from  the  important,  functional  stand- 
point it  is  far  from  being  tlie  true  state  of  the  cases. 

In  this  group  there  is  marked  hypertrophy  and  moderate 
dilatation  of  the  left  ventricle  with  dilatation  and  nodular 
sclerosis  of  the  aorta.  The  kidneys  are  firm,  red,  small, 
coarsely  granular,  the  cortex  much  reduced,  the  capsule 
adherent.  Cysts  are  connnon.  Tt  is  the  familiar  primary 
contracted  kidney.  ^NFaHory  calls  this  cai)snhii'-glomei-ulo- 
nephritis.  The  etiology  is  ()])scure.  Often  no  cause  can  ])e 
found.  Again,  there  is  a  history  of  some  kidney  involve- 
ment following  one  of  tlie  acute  infectious  diseases,  or  it 
may  follow  the  ne])hritis  of  ])regnancy.     Usually,  however. 


114  ARTERIOSCLEROSIS 

tlioso  cases  fall  into  the  ^roup  of  secondary  contracted  kid- 
neys, chronic  parenchymatons  nephritis. 

Illustrative  CiiHv. — E.  Z.,  a  woman,  aj^x^d  tliiity-six  years,  was  seen  July  26, 
1916,  in  coma.  There  uas  a  history  of  typhoid  fever  at  nineteen  years,  but  no 
other  disease.  She  had  had  nine  full-term  pregnancies,  the  last  one  thirteen 
months  previously.  For  a  week  before  the  onset  of  the  present  illness  she  had 
eomi)lained  of  severe  headaches  and  dizziness.  There  were  no  heart  symptoms. 
For  the  past  year  she  has  had  nycturia.  Physical  examination  revealed  tubular 
breathing  beneath  the  manubrium,  a  few  rales  in  the  chest,  an  enlarged  heart 
(left  side),  with  a  systolic  murmur  over  the  aortic  area.  Blood  pressure  was 
178-125-53,  the  pulse  rate  96,  leucocytes  27,250.  Venesection  of  500  c.c.  of 
blood  and  intravenous  injections  of  500  c.c.  of  5  per  cent  NaHCOg  in  normal 
saline  were  employed.  Lumbar  puncture  withdrew  60  c.c.  of  clear  fluid  under 
pressure  with  6  cells  per  cubic  millimeter.  The  eye  grounds  showed  distinct 
haziness  of  the  disks  and  dilatation  of  the  veins.  Blood  pressure  after  vene- 
section was  164-122-42,  i>ulse  76,  but  in  a  few  days  rose  to  222-142-80,  pulse  70. 
A  second  venesection  of  400  c.c.  and  proctoclysis  of  1000  c.c.  saline  solution 
was  tried.  Tlie  blood-pressure  now  was  198-140-58.  The  pH  of  the  blood  was 
7.6,  the  alkaline  reserve  was  .'^i5  volume  per  cent  (van  Slyke),  and  the  CO. 
tension  of  the  alveolar  air  (Marriott)  was  25  mm.  The  i)lithalein  on  the  day 
following  the  second  venesection  was  45  per  cent  in  two  hours.  The  urine 
at  first  showed  500  c.c.  in  twenty-four  hours,  specific  gravity  1016,  albumin 
and  casts.  Later  she  passed  LiOO  to  1600  c.c.  with  specific  gravity  around 
1010.  The  blood-pressure  fluctuated  considerably,  reaching  as  low  as  138-98- 
40,  pulse  88.  She  was  discharged  improved  September  10,  1916.  She  had 
constant  headache  but  managed  to  keep  up.  In  June,  1917,  she  suddenly 
died  in  an  uremic  coma. 

Groujo  B.  This  one  might  designate  as  the  hereditary 
type,  although  there  is  not  always  a  history  in  the  ante- 
cedent. This  group  includes  the  robust,  florid,  exuberantly 
healthy  people.  They  often  are  heard  to  boast  that  they 
have  never  had  a  doctor  in  their  lives.  They  are  usually 
thick-set  or  very  large,  fleshy  people.  The  pressure  pic- 
ture is  exceedingly  high.  The  pulse  pressure  is  moderately 
increased.  The  arteries  are  rather  large,  fibrous,  and  often 
quite  tortuous,  although  this  is  not  always  the  case.  Some 
persons  have  hard,  small,  fibrous  arteries.  There  is  no 
puffiness  beneath  the  eyes,  no  polyuria,  and  no  nycturia  as 
a  rule.  The  urine  is  of  normal  amount,  color,  and  specific 
gravity.  Albumin  is  only  rarely  found  and  then  in  traces, 
but  careful  search  of  a  centrifuged  specimen  invariably  re- 


PHYSIOLOGY    OF    THE    CIRCULATIOX  11.") 

veals  a  few  hyaline  casts.  The  phthaloiii  excretion  is  nor- 
mal or  only  slightly  rednced.  Tlie  kidneys  excrete  salt  and 
nitrogen  normally.  It  is  in  this  group  that  apoplexy  is 
found  most  frequently.  The  rupture  of  tlie  vessel  occurs 
Avhen  tlie  victim  is  in  pei'fect  health,  often  ^Yithout  any 
Avarning.  Occasionally  when  such  a  case  recovers  suffi- 
ciently to  be  around,  cardiac  decompensation  sets  in  later 
and  he  dies  then  of  the  cardiac  complications. 

Pathologically  the  hearts  of  such  persons  are  found  to 
have  the  most  enormous  hypertrophy  of  the  wall  of  the  left 
ventricle.  The  cavity  is  somewhat  enlarged,  as  is  always 
the  case  when  the  pulse-pressure  is  increased,  but  the  size 
of  the  cavity  is  not  the  striking  feature.  The  aorta  is 
fibrous,  thick  walled,  and  the  arch  is  slightly  dilated.  There 
are  patches  of  arteriosclerosis.  One  such  case  seen  only 
at  autopsy  had  a  rupture  of  the  aorta  just  above  the  sinus 
of  Valsalva  and  died  of  hemopericardium.  The  kidneys 
are  of  normal  size,  dark  red,  firm,  the  capsule  strips  readily, 
the  surface  is  smooth  or  finely  granular,  the  cortex  is  not 
decreased.  The  pyramids  are  congested  and  red  streaks  ex- 
tend into  the  cortex.  Microscopically  the  capsules  of  the 
glomeruli  are  a  trifle  thickened;  a  few  show  hyaline 
changes.  There  is  rather  diffuse,  mild,  round-cell  infiltra- 
tion between  the  tubules.  The  tubular  ei:)itheliuni  shows  lit- 
tle or  no  denionstra])le  changes.  The  arterioles  are  gener- 
ally the  seat  of  a  moderate  thickening  of  the  intima  and  me- 
dia, but  it  is  not  usual  to  find  obliterating  endarteritis. 
There  is  evidently  a  diffuse  fibrous  change  which  has  not 
affected  either  the  tubules  or  glomeruli  to  any  great  extent. 

Illustrative  Case. — L.  C,  a  man,  aged  fifty-six  years,  stonemason  by  trade, 
is  a  stocky,  thick-necked  individual.  He  had  never  been  ill  in  his  life  until 
a  year  ago,  when  he  fell  from  his  chair  unconscious.  He  had  a  right-sided 
hemiplegia  wliich  has  cleared  up  so  completely  that  except  for  a  very  slight 
drag  to  his  foot  he  walks  perfectly  well.  He  came  in  complaining  of  short- 
ness of  breath  and  cough.  There  Avas  no  swelling  of  the  feet.  Here  evi- 
dently was  left-heart  decompen.sation.  Examination  showed  the  blood  pressure 
to  be  240-130-110,  pulse  irregular,  104  to  the  minute.  There  were  cyanosis 
and    rales   throughout    l)oth    chests.     The    urine    was    normal    in    color,    specific 


]  1  6  ARTERIOSCLEROSIS 

gravity  102'),  small  amount  of  albumin,  few  casts,  hyaline  and  granular. 
The  phthalein  elimination  was  65  per  cent  in  two  hours.  Under  rest,  purga- 
tives, and  digitalis  he  was  much  improved.  He  has  since  had  two  other 
ajjoplectic  strokes,  the  last  of  which  was  fatal. 

Wlien  these  patients  are  seen  with  acute  cardiac  decom- 
pensation, there  are,  of  course,  mucli  albumin  and  many 
casts  in  the  urine,  and  the  plithalein  output  is,  for  the  time 
being,  decreased. 

Group  C.  Tliis  might  ])e  called  the  arteriosclerotic  high- 
tension  group  (Stone's  cardiac  group).  The  cases  are  usu- 
ally over  fifty  years  old.  They  are  men  and  women  who 
have  lived  high  and  thought  hard.  Often  they  have  had 
periods  of  great  mental  strain,  ]\Iany  men  in  this  group 
were  athletes  in  their  young  manhood.  Many  have  been 
fairly  heavy  drinkers,  although  never  drinking  to  excess. 
They  are  usually  well  nourished  and  inclined  to  stoutness. 
The  pressure  picture  is  high  systolic  with  normal  or  only 
slightly  increased  diastolic  and  large  pulse  pressure.  The 
arteries  are  large,  full,  fibrous,  usually  tortuous.  The  heart 
is  very  large,  the  apex  far  down  and  out.  There  is  no  poly- 
uria; nycturia  is  uncommon,  quite  the  exception.  The  urine 
is  normal  in  color,  amount,  and  specific  gravity.  Albumin 
is  only  rarely  found  and  hyaline  casts  are  not  invariably 
present.  The  plithalein  excretion  is  quite  normal  and  the 
excretions  of  salt  and  nitrogen  are  also  normal.  The  ter- 
minal condition  in  most  of  the  patients  in  this  group  is  car- 
diac decompensation.  They  may  have  several  attacks  from 
which  they  recover,  but  after  every  attack  the  succeeding 
one  is  produced  by  less  exertion  than  the'preceding  one,  and 
it  becomes  more  and  more  difficult  to  control  attacks. 
Eventually  the  patients  become  bed-  or  chair-ridden,  and 
finally  die  of  acute  dilatation  of  the  heart. 

Occasionally  patients  in  this  group  may  have  a  cerebral 
attack,  l)ut  in  my  experience  this  is  uncommon.  Pathologi- 
cally the  heart  is  large,  at  times  ti'ue  cor  hovnuDn,  dilated 
and  hypertropliied,  Tlie  cavity  of  the  left  v(mtricle  is  much 
dilated.    The  aorta  is  dilated  and  sclerosed. 


PHV.SIOr.OGV    OF    THE    CHICTLATIOX  117 

The  kidneys  are  increased  in  size,  are  firm,  dark  red 
in  color,  with  fatty  streaks  in  the  cortex.  The  capsule  strips 
readily  and  the  cortex  is  normal  in  thickness  or  only 
slightly  increased.  The  organ  offers  some  resistance  to  the 
knife.  The  microscope  shows  small  areas  scattered 
throughout  where  the  glomeruli  are  hyalinized,  the  stroma 
full  of  small  round  cells,  the  tubules  dilated,  and  the  cells 
are  almost  bare  of  protoplasm.  Naturally  the  tubules  are 
full  of  granular  cast  material.  Also  the  arterioles  show 
extensive  intimal  thickening,  fibrous  in  character,  with  oc- 
casional obliterating  endarteritis.  One  gets  the  impression 
that  the  small  sclerotic  lesions  are  the  result  of  anemia  and 
gradual  replacement  of  scattered  glomeruli  by  fibrous  tis- 
sue. For  the  most  part  the  kidney,  except  for  the  chronic 
passive  congestion,  appears  quite  noi'mal.  One  can  readily 
understand  that  in  such  a  kidney  function  could  not  have 
been  much  interfered  with. 

Illustrative  Case. — C.  K.,  an  active,  stout,  business  man,  aged  fifty-six 
jears,  consulted  me  on  account  of  shortness  of  breath  and  swelling  of  the  feet 
in  May,  191o.  He  had  just  returned  from  a  hospital  in  another  city,  where 
he  had  gone  with  what  was  apparently  cardiac  decompensation.  In  his  early 
uianhood  he  had  been  a  gymnast  and  a  prize  winner.  He  has  worked  hard, 
often  given  way  to  violent  paroxysms  of  temper,  has  eaten  heavily  but  drunk 
very  moderately.  The  heart  was  greatly  enlarged,  the  arch  of  the  aorta 
dilated,  a  mitral  murmur  was  audible  at  the  apex.  Tiie  radials  and  tem])orals 
were  large,  tortuous,  and  fibrous.  The  blood  pressure  picture  ranged  around 
180-90-90.  He  was  easily  made  dyspneic  and  had  a  tendency  to  swelling  of 
the  lower  legs.  The  urine  was  acid,  of  normal  specific  gravity',  normal  in 
amount,  normal  phthalein,  normal  concentration  of  salt  and  nitrogen,  con- 
tained albumin  only  when  he  was  suffering  from  decompensation  of  the  heart. 
Casts  were  always  found.  He  finally  died,  after  sixteen  months,  with  all 
the  .symptoms  of  chronic  myocardial  insufficiency.  The  heart  Avas  enormous, 
a  true  cor  hovi)iuw.  The  kidneys  were  typical  of  this  condition,  possildy 
somewhat  larger  than  usual. 

Hypotension 

AVhen  the  pressure  is  constantly  Ix'low  the  normal,  it  is 
called  hypotension.  This  may  l)e  Iransieiit — as  in  fainting 
— it  mav  l)e  a  normal  state  of  tlie  individual,  it  occui's  in 


118 


AKTEIUOSCLEIIOSIS 


most  I'evi'is  and  in  a  i'l'eat  variety  of  diseases,  including- 
anemias. 

In  arteriosclerosis,  especially  tlie  diffuse  (senile)  type, 
tlie  l)lood  pressiii-e  is  invariably  low,  and  may  be  spoken  of 
as  hypotension.  The  lieart  in  sucli  a  case  is  small,  the 
muscle  is  flabby,  there  is  brown  atrophy  of  the  fibers,  and 
some  replacement  of  the  muscle  cells  by  connective  tissue. 
The  same  causes  which  have  produced  general  arterioscle- 
I'osis  have  also  produced  sclerosis  of  the  coronary  arteries, 
and  probably  the  lessened  blood  supply  accounts  for  nuich 
of  the  atrophy  of  the  heart  muscle. 

In  typhoid  fever  the  maximum  blood  j^i'essure  during 
beginning  convalescence  may  be  as  low  as  65  nnn.  Hg.  T 
have  freciuently  seen  hypotension  of  80  mm.  This  is  com- 
mon. 

jMeningitis  is  the  only  acute  infectious  disease  in  which 
the  blood  pressure  is  more  often  high  than  low.  This  is 
accounted  for  by  the  increased  intracranial  tension. 

Following  large  hemorrhages  the  blood  pressure  is  re- 
duced. In  venesection  the  withdrawal  of  blood  may  not 
affect  the  l)lood  pressure.  The  procedure  is  done  to  relieve 
overdistension  of  the  heart. 

In  pleurisy  with  effusion  and  in  pericarditis  with  effusion 
there  is  hypotension. 

Collapse,  whetlier  from  poisoning  by  drugs  or  as  the  re- 
sult of  dysentery,  cholera,  or  profuse  vomiting  from  what- 
ever cause,  reduces  the  blood  pressure. 

In  cachectic  states,  such  as  cancer,  the  blood  pressure  is 
low.  (leneral  Avasting  of  the  whole  nmsculature  includes 
that  of  the  heart  and  the  li(»art  nmscle  shows  the  condition 
known  as  "brown  atrophy." 

A  most  interesting  and  important  coiulition  in  which 
hypotension  occurs  is  pulmonary  tu])erculosis.  Haven 
Emerson  lias  recently  gone  over  the  whole  su])ject  in  a  care- 
ful piece  of  work  and  his  snnmiary  is  as  follows: 

"Hypotension   or   subnormal   blood   i)ressure   is   univer- 


J 


PHYSIOLOGY    OF    THE    CIRCTLATIOX  119 

sally  found  in  advancod  puliiionai'v  tuberculosis,  in  wliicli 
condition  emaciation  may  play  a  pai't  in  its  causation. 
Hypotension  is  found  in  almost  all  cases  of  moderately  ad- 
vanced tuberculosis,  or  in  early  cases  in  wliicli  the  toxemia 
is  marked  excei)t  when  arteriosclerosis,  the  so-called  ar- 
thritic or  ft'outy  diathesis,  chronic  nephritis,  or  diabetes 
complicate  the  tuberculosis  and  ])ring'  about  a  normal  pres- 
sure or  a  hypertension.  Occasionally  the  period  just  pre- 
cediui^'  a  hemoptysis  or  durino-  a  hemoptysis  may  show  hy- 
pertension in  a  patient  whose  usual  condition  is  that  of 
hypotension. 

"Hypotension  has  been  found  ]jy  so  many  observers  in 
early,  doubtful  or  suspected  cases  with  or  before  physical 
signs  of  the  disease  in  the  lungs,  and  is  considered  by  com- 
petent clinicians  so  useful  a  dilferential  sign  between  vari- 
ous conditions  and  tuberculosis,  that  it  should  1)e  sought  for 
as  carefully  as  it  is  the  custom  at  present  to  search  for 
pulmonary  signs. 

"Hypotension  when  found  persistently  in  individuals  or 
families  or  classes  living  under  certain  unhygienic  condi- 
tions should  put  us  on  our  guard  against  at  least  a  pre- 
disposition to  tuberculosis.  Most  unhygienic  conditions, 
overwork,  undernourishment  and  insufficient  air,  are  of 
themselves  causes  of  a  diminished  resistance,  and  it  seems 
likely  that  a  failure  of  normal  cardiovascular  response  to 
exercise  or  change  of  ])osition  may  be  found  to  indicate  this 
stage  of  susceptil)ility,  especially  to  tuberculous  infection. 

"...  Hypotension,  when  it  is  present  in  tuberculosis,  in- 
creases with  an  extension  of  the  process.  Recovery  from 
hypotension  accompanies  arrest  or  improvement.  Eeturn 
to  normal  pressure  is  conunonly  found  in  tliose  who  are 
cured.  Continuation  of  hypotension  seems  never  to  accom- 
pany improvement.  Prognosis  can  as  safely  be  based  on 
the  alteration  in  the  blood  ])ressui-e  as  on  changes  in  the 
pulse  or  tem])erature.     .     .     ." 

Thei-e  are  a  few  drugs  which  lower  the  blood  pressur(\ 


120 


ARTERIOSC'LEKOSIS 


but,  as  a  rule,  llieir  effects  are  more  or  less  transitory.  We 
know  of  no  dru^',  unless  it  })e  iodide  of  potassium,  Avliieli  lias 
the  property  of  causing  changes  in  the  blood  (decrease  in 
viscosity?),  which  tends  to  reduce  the  blood  pressure  when 
it  is  excessive.     This  drug  fails  us  many  times. 

80VIE   I1RUG8   WHICH   INFLUENCE   THE  BLOOD  PRESSURE 


Pressure  Raisers 

Adrenalin,  when  injected  directly 
into  a  vein  or  deep  into  the  muscles. 
The  action  is  transitory. 

Caffeine,  preferably  in  the  form 
of  eaffeine-sodium-benzoate.  A  good 
drug. 

Strychnine,  ^vllich  does  not  act  di- 
rectly but  seemingly  through  the 
higher  centers. 

Ergot,    somewhat    uncertain. 

Nicotine,  not  used  therai)eutically. 

Camphor,  used  in  sterile  olive  oil 
and  injected  deejily  into  the  muscles. 

Digitalis,  when  the  cardiac  tone  is 
low  and  decompensation  is  present. 
Its  action  is  prolonged  but  slow.     In- 


jections of  the  infundibular  portion 
of  the  pituitary  body.  Not  in  use 
clinically. 

Pressure  Depressors 

Nitroglycerine  and  amyl  nitrite, 
action  transitory  but  rapid. 

Sodium  nitrite  and  erythrol  tetra- 
nitrate.  Action  somewhat  more  pro- 
longed. 

Aconite,  veratrum  viride,  chloral, 
etc.     These  depress  the  heart. 

Purgatives,  drastic  and  iiydragoguc. 

Potassium  and  sodium  iodide  may 
lower  blood  pressure.  W^hen  they  do, 
the  action  is  prolongi-d. 

Diuretin  and  theocin-sodium-ace- 
tate. 


Venous  Pressure 

Comparatively  little  work  has  been  done  upon  the  de- 
termination of  the  pressure  in  the  veins  in  man.  It  is  con- 
ceivable that  this  procedure  may,  at  times,  be  of  great 
value.  A  number  of  attempts  have  ])een  made  to  measure 
the  venous  pressure  by  compressing  the  arm  veins  and  not- 
ing on  a  manometer  tlie  force  necessary  to  obliterate  tlie 
vein.  As  the  pressure  is  so  slight,  water  is  used  instead 
of  mercury,  and  readings  have  been  given  in  centimeters 
of  water. 

In  the  apparatus  shown  in  the  figure  (Fig.  33),  ])rs. 
Hooker  and  Eyster  succeeded  in  making  estimations  of  the 
venous  pressure.  The  box  B  is  held  in  position  by  the  tapes 
A,  so  that  the  vein  is  visible  through  the  rectangular  open- 
ing in  the  thin  rubber  covering  the  bottom.  The  box  is  con- 
nected with  the  water  manometer  G,  by  a  rul)ber  tube, 
from  Avhich  a  T-tube  enters  the  rubber  bulb  K.  AVhen  the 
bulb  E  is  compressed  between  the  plates  D,  by  the  coarse 


pnvsioi.()(;v  ok  the  (Miutlatiox 


1L>1 


thiimJjscrcw  (',  air  is  i'orced  into  tlio  l)ox  />,  cxcrtiiii!,'  a  pres- 
sure on  the  vein  lying  exposed  l)eneatli.  This  pressure  is 
transmitted  directly  to  the  nianonieter  G,  and  may  be  read 
off  in  centimeters  of  water  on  the  accompanying  scale.  The 
veins  of  tlie  back  of  the  hand  are  used  and  there  must  be  no 


l-'ii,'.  M- — A|)])aratus  fur  estimating  tin-  voiious  lilood  iire.-^siirc  in  man,  dcviM'il  l)y 
I  Irs.  Iliioker  and  Ivyster.  The  small  tigmc  is  the  detail  of  the  hox  11.  S<e  explanation 
in   text. 


obstruction  between  them  and  the  heart.  The  rubber-cov- 
ered box  is  accurately  and  lightly  fitted  over  a  vein  and 
])rossure  made  until  it  is  obliterated.  By  measuring  the 
distance  above  or  below  the  heart  level  that  the  hand  was 
when  the  obsei-vation  was  nuidc.  and  subtracting'  or  adding 


122 


AKTERIOSCLEROSLS 


these   fi<2,'iires   to   the   iiiaiiometer    I'eadliii^',   Ave    obtain   the 
venous  pressure  at  tlie  heart  level. 

Eyster  has  modified  this  instrument  so  that  it  is  now 
nnieh  simpler  to  operate,  lie  uses  a  small  glass  cup  with  a 
flaring  edge  and  a  diameter  of  about  2  em.  This  is  sealed 
to  the  skin  directly  over  a  vein  on  the  back  of  the  hand  by 
means  of  collodion.  The  stem  of  the  cup  has  a  rubber  tube 
leading  to  a  small  hand  bulb  and  to  the  manometer  tube 


Fig.   34. — New  vei.ous  pressure   instrument.    (After   Kystcr.) 

which  contains  colored  water.  Slight  compression  of  the 
hand  bulb  obliterates  the  vein  Avhich  can  be  seen  through 
the  glass  cup.  The  pressure  in  centimeters  of  water  is  then 
read  off.  (Fig.  34.)  The  principle  is  the  same  as  in  the 
earlier  instrument,  but  the  application  is  easier. 

Practically  Hooker  and  Eyster  found  that  the  normal 
variation  in  healthy  subjects  was  from  3  to  10  cm.  of  w^ater. 
The  pressure  rose  in  cases  of  decompensated  hearts  with 


PHYSIOLOGY    OF    THE    CIRCULATIOX  123 

dyspnea  and  venous  stasis,  and  returned  to  normal  with 
improvement  in  the  condition  of  the  patient.  It  might  be 
possible  with  this  instrument  to  foretell  an  onccmiing'  de- 
compensation by  the  rise  in  venous  pressure. 

The  venous  pressure  may  also  be  estimated  roughly  by 
slowly  elevating  the  arm  and  noting  the  instant  at  which 
a  particular  vein  collapses.  By  measuring  the  height  of 
the  vein  above  the  heart  some  idea  may  be  obtained  of  the 
pressure  within  the  right  auricle. 

The  Pulse 

There  is  nothing  characteristic  about  the  pulse  of  a 
person  suffering  from  arteriosclerosis,  except  it  be  the  dif- 
ference in  the  pulse  of  high  tension  and  of  low  tension. 
The  pulse  of  high  tension  has  a  gradual  rise,  a  more  or  less 
rounded  apex,  and  the  dicrotic  wave  is  slightly  marked  and 
occurs  about  half-way  down  on  the  descending  limb.  In 
arteriosclerosis  with  low  tension  the  radial  artery  is  usually 
so  rigid  that  very  little  pulse  wave  can  be  obtained.  The 
general  form  of  a  low  tension  pulse  is  a  sharp  up-stroke,  a 
pointed  summit,  and  a  secondary  wave  on  the  base  line, 
which  corresponds  to  the  dicrotic  wave.  Such  a  pulse  can 
be  easily  palpated,  and  is  known  as  a  dicrotic  pulse.  How- 
ever, such  a  pulse  can  occur  only  when  the  artery  still  re- 
tains all  or  a  large  part  of  its  elasticity;  hence  in  arterio- 
sclerotic low  tension  we  would  never  see  such  a  i)ulse  as 
the  typical  dicrotic. 

The  Venous  Pulse 

It  would  carry  us  too  far  to  discuss  fully  the  character 
of  the  venous  pulse,  but  a  brief  summary  of  the  essential 
features  of  the  normal  venous  pulse  is  presented.  The 
venous  pulse  is  a  term  used  to  express  the  tracing  obtained 
from  the  internal  or  external  jugular  vein  at  the  root  of 
the  neck.  Xormally  a  very  characteristic  curve  is  ])roduced, 
which  can  be  readilv  analvzed  into  a  series  of  waves  corre- 


124 


AKTEltlOSCLEROSrS 


spoiidiiig  to  the  fluctuations  in  the  cardiac  cycle.  To  under- 
stand these  waves  and  their  values,  the  accom]3anying 
fi<j,ure  is  lielpful.     (Fig.  35.) 

Bachmann  sunmiarizes  the  normal  waves  in  the  venous 
pulse  tracing  as  follows: 

''The  physiological  or  so-called  venous  pulse  consists  of 
three  positive  and  three  negative  waves,  bearing  a  more  or 


Fig.  35. — Semidiagranimatic  ifpiLscntation  of  the  events  in  the  cardiac  cycle:  JiiR-, 
pulse  in  the  jugular  vein;  Aur.,  contraction  of  auricle;  \'.  Pr.,  intraventricular  pres- 
sure; Pap.  M.,  contraction  of  the  i)apillary  muscles;  Car.,  carotid  jnilse.  Below  are 
given  the  times  of  occurrence  of  the  heart  sounds  and  of  the  opening  and  closing  of 
the   heart   valves.      (After   Ilirschfelder.) 


less  definite  relation  to  the  events  of  the  cardiac  cycle,  and 
having  their  origin  in  the  various  movements  of  the  cham- 
bers and  structures  of  the  right  heart.  The  first  positive 
wave  (a)  is  presystolic  in  time,  and  is  due  to  the  contrac- 
tion of  the  auricle,  causing  a  slowing  of  the  venous  current 
and  producing  a  centrifugal  wave  through  a  sudden  arrest 
of  tlie  inflowing  ])lood.  The  second  positive  wave  (S)  is 
presystolic  in  time,  and  originates  in  the  sudden  projection 


PHYSIOLOGY    OF    TflE    CIRCTLATIOX 


125 


of  the  tricuspid  valve  into  the  cavity  of  the  auricle  during 
the  quick,  incipient  rise  in  the  intraventricular  pressure 
occurring-  in  the  protosystolic  period.  The  third  positive 
wave  (r)  occurs  toward  the  end  of  venti'icular  systole.  It 
consists  of  two  lesser  waves  separated  by  a  shallow  notch. 
The  factors  entering  into  its  formation  are  the  relaxation 


Carotid 


mmmmm'Bmmmm^um 


Fig.    36. — Simultaneous  tracings   cf   the   jugular   and   carotid   pulses   showing   normal   wave; 
in   the  venous  pulse  and   relation   to  carotid  pulse.      (After   Rachmann.') 


r^y    uu 


!\^.J\       n(i     J\\     \  :    \f\\     r^.       -'ill     ^.   k 


X  >  \y 


Fig.  37. — Jugular  and  carotid  tracing  from  a  normal  individual  with  a  well-niarke<l 
third  heart  sound  showing  a  large  "h"  and  a  smaller  i)re-auricular  wave  "w."  ?  indi- 
cates a  small  wave  in  mid-diastole  following  the  "h"  wave,  occasionally  found  though 
perhaps   an    artefact.      (.\fter    Ilirschfelder. ) 

of  the  papillary  muscle  at  a  time  when  the  intraventricular 
is  still  higher  than  the  intraauricular  pressure,  resulting 
in  an  upward  movement  of  the  tricus])id  leaflets  and  a  re- 
turn of  the  auriculoventricular  septum  to  its  position  of 
rest. 


126  ARTERIOSCLEltOSIS 

"The  first  negative  Avave  (l)etwecii  positive  wave  a  and 
*S')  is  due  to  the  relaxing  auricle.  The  second  negative 
wave  (Af)  occurs  during  the  diastole  of  the  auricle.  It 
is  due  to  the  dilatation  of  its  walls,  to  the  displacement  of 
the  auriculoventricular  septum  toward  the  apex  occurring 
at  the  time  of  ventricular  systole,  and  to  the  pull  of  the 
papillary  nmscles  on  the  tricuspid  valve  leaflets.  The  third 
negative  wave  (17)  appears  during  ventricular  diastole  and 
in  the  common  pause  of  the  heart  chambers.  Its  cause  is 
found  in  the  passage  of  the  blood  from  the  auricle  into  the 
ventricle.  It  is  somewhat  modified  possibly  by  the  contin- 
ual ascent  of  the  auriculoventricular  septum  and  by  a  wave 
of  stasis  due  to  the  accumulation  of  blood  coming  from  the 
periphery."     (Fig.  36.) 

Hirschf elder  has  described  another  wave  which  he  calk 
the  ^'h"  wave,  which  is  due  to  the  floating  up  of  the  tricus- 
pid valve  by  the  blood  in  the  ventricle  before  the  complete 
filling  of  the  ventricle  following  the  auricular  svstole.  (Fig. 
37.) 

The  Electrocardiogram 

In  the  past  few  years  an  immense  amount  of  work  has 
been  done  by  numerous  observers  on  the  changes  in  the 
electrical  potential  of  the  various  portions  of  the  heart 
during  contraction.  The  very  elaborate  and  delicate  elec- 
trocardiograph with  the  string  galvanometer  devised  by 
Einthoven  is  used.  It  has  been  definitely  determined  that 
the  impulse  to  cardiac  contraction  originates  in  the  sinus 
node,  a  collection  of  differentiated  nerve  cells  situated  at 
the  junction  of  the  superior  vena  cava  with  the  right  auricle. 
From  there  the  impulse  travels  in  certain  fibers  in  the  in- 
terauricular  wall,  passes  through  another  node,  the  auric- 
uloventricular or  Tawara  node,  situated  in  the  auricular 
wall  just  above  the  auriculoventricular  ring,  thence  via 
the  Y-])undle,  or  bundle  of  His  to  the  ventricles.     This  se- 


PHVSIOLCKJV    OF    TMK    CIRCULATIOX 


127 


qiienee  is  ord(M-ly,  regular,  and  normally  invariable.     (Fig. 
38.) 

The  sino-auricular  (s-a)  node  is  the  most  irritable  por- 
tion of  the  heart,  it  is  endowed  with  the  greatest  amount 


Left 
vagus 


Sino-auricular  node 


^    ^J^ 


Centres  of  ventricular 
contraction 


Tawara's  node 
His'  liundle 


Centre?  of  ventricular  contraction 


I'ig.  38. — Right  side  of  the  luart  showing  diagraniniatically  the  distribution  of  tlu' 
two  vagus  nerves  to  different  |)arls  of  tlic  visciis.  The  impulse  to  contraction  oriijinales 
at  the  sino-auricular  node  and  passes  over  the  wall  of  the  auricle  to  Tawara's  node,  and 
thence  over  His"  bundle  across  the  auriculoventricular  septum  to  be  distributed  through- 
out the  ventricular  wall.  If  the  upiier,  sino-auricular,  node  is  damaged,  or  if  its  im- 
pulses fail  to  get  across  the  wall  of  the  auricle,  Tawara's  node  acts  in  its  place  to  start 
off  the  ventricle.  If  a  lesion  at  the  base  of  the  mesial  segment  of  the  tricuspid  valve 
damages  His'  bundle,  so  that  Tawara's  node  is  cut  ofi'  from  the  ventricle,  then  tlie  ven- 
tricle   may    originate   its    own    imp\ilscs    to    contraction.       (Hare's    I'ractice    of    .Medicine.) 


128 


ARTKItlOSCLEROSlS 


l.c.'ul    I     (right    anil  — k-ft    ami; 


-i.^.r:~ii r:  v 

"  ■    -  - 

"■-•"["' 

:     I       ■— T—  - 

1        t --- i-.  - 

z=h 

■: ;- 

-  ■-  ■- j- -— — 

"L±"' 

.  ,_4 — ^. ^—i — T 

^ySw^^'^^wiii*^^ 

I] 

Mi 

ii|^ji'taP^|j*%M^ 

_-^  „.I — ^  'j  : 

J — „„_^ — . , 

bii^                                                       1 

"P  -H     s     O  .t  if      Sfr^tt/L. 

•  •••       ••  ^a*                      «* 

iSJSSS^ 

Lead    II    (right    arm — left    log) 


I, cad    III    (k-ft    arm — left    kg). 
I''ig     .i9. — Normal    electrocardiogram.      (After    Ilart.) 


PirVSIOLOOV    OF    TTTK    ClRCrLATIOX  129 

of  rliytlimicity  as  well.  It  is  uiider  the  control  of  the  vagus 
nerve.  Its  inherent  rate  of  rliytlimicity  is  i)robably  more 
rapid  than  the  usual  numbers  of  impulses  per  minute,  but 
it  is  inhibited  by  the  vagus.  Paralysis  of  the  vagus  endings 
increases  the  rate  of  impulse  formation  and  therefore  the 
rate  of  the  heart. 

The  electrocardiogram  is  a  graphic  representation  on  a 
photographic  film  or  sensitive  bromide  paper  of  the  changes 
of  electrical  potential  during  muscular  activity.  The  lines 
are  made  by  the  highly  magnifiiHl  sti'ing  of  the  galvanom- 
eter as  it  moves  across  the  slit  in  the  photographic  appa- 
ratus in  response  to  the  induction  currents  set  up  in  the 
heart  magnified  by  the  special  galvanometer. 

The  record  is  made  in  three  so-called  Leads. 

Lead  I 
The  electrodes  are  attached  to  right  arm  and  left  arm. 

Lead  II 
The  electrodes  are  attached  to  right  arm  and  left  leg. 

Lead  III 
Tlie  electrodes  are  attached  to  left  arm  and  left  lep;. 

A  series  of  regular  figures  is  normally  obtained  in  Avhicli 
are  depressions  and  elevations  and  regular  spacing  of  these 
elevations  and  depressions.  The  waves  so-called  have  been 
arbitrarily  designated  P,  Q,  R,  S,  T.  There  is  some  dif- 
ference in  the  three  leads.  "The  wave  P  is  positive  in  all 
leads.  P  to  R  interval  varies  slightly  in  the  fJiree  leach. 
All  the  Avaves  of  Lead  II  are  greater  than  those  of  Leads  I 
and  ///.  The  wave  R  is  positive  in  all  leads.  T  is  usually 
positive  in  all  leads,  but  is  occasionally  negative  in  Lead 
III.  Even  in  normal  individuals  there  is  a  considerable 
range  of  variation  in  the  electrocardiogram  which  is  within 
the  limits  of  the  normal."     (Hart.)     (Fig.  39.) 

The  P  wave  is  admitted  to  be  the  wave  of  auricular  con- 
traction.   Q,  R,  S,  is  the  ventricular  complex  caused,  it  is 


130  AKTEPJOSCLEPiOSTS 

tlioii^'lit,  l)y  tlio  ciirroiit  passiii"-  ovor  the  ventricles.  T 
wave  is  not  yet  definitely  settled.  It  lias  been  thought  by 
some  that  it  represented  actual  ventricular  contraction  and 
its  height  and  shape  had  some  meaning  in  heart  force. 
This  is  denied  by  others.  Hart  defines  it  as  ''The  final  ac- 
tivity of  the  ventricle."  The  T  wave  is  usually  increased 
in  size  during  exercise. 

The  P-R  interval  is  almost  the  most  important  feature 
of  the  tracing.  It  is  the  actual  conduction  time  in  fractions 
of  a  second  of  the  impulse  from  s-a  node  to  the  ventricles. 
Normally  this  is  about  0.2  second  or  slightly  less.  Much 
that  was  hoped  for  from  the  electrocardiograph  in  the  clinic 
has  not  been  forthcoming.  Its  greatest  value  is  in  states 
of  abnormal  conductivity,  such  as  various  grades  of  heart 
block,  extra-systoles,  whether  originating  in  auricles  or  in 
either  ventricle,  abnormalities  of  rhythm,  as  flutter  and 
fibrillation.  It  has,  however,  aided  materially  in  the  in- 
telligent interpretation  of  many  phenomena  heretofore  not 
well  understood,  and  has  enormously  increased  our  knowl- 
edge of  the  physiology  and  pathologic  physiology  of  the 
heart. 

It  is  not  possible  to  enter  farther  into  the  subject  here. 
This  brief  discussion  must  suffice.  The  reader  is  referred 
to  works  on  this  subject  in  connection  with  diseases  of  the 
heart. 


CHAPTER  IV 

IMPORTANT    CARDIAC    IRREGULARITIES 
ASSOCIATED  WITH  ARTERIOSCLEROSIS 

Arteriosclerosis  of  the  aorta,  of  the  coronary  arteries, 
or  of  both,  is  practically  always  found  in  cases  dying  of 
various  cardiac  irregularities  other  than  those  the  result 
of  rheumatic  cardiac  lesions.  It  is  not  that  arteriosclerosis 
causes  the  cardiac  lesions  (although  the  thickening  of  the 
walls  of  the  coronary  arteries  does  interfere  mechanically 
with  the  nutrition  of  the  heart  muscle),  but  the  arterio- 
sclerosis is  a  part  of  the  tissue  reaction  in  the  arteries  to 
some  set  of  causes  affecting  the  whole  body.  It  is  true 
when  one  boils  down  the  question  to  its  last  analysis,  gen- 
eral arteriosclerosis  may  mechanically  so  interfere  with  the 
blood  supply  to  tissues  that  the  tissue  is  thrown  out  of 
function  either  in  the  reduction  or  even  loss  of  function. 
So  it  may  be  that  occasionally  the  arteriosclerosis  in  the 
arteries  supplying  the  heart  is  really  responsible  for  the 
cardiac  irregularity.  The  past  few  years  have  been  fruit- 
ful ones  in  increasing  our  knowledge  of  the  various  irregu- 
larities of  the  heart.  We  can  do  no  more  than  sketch 
briefly  some  of  them  in  relation  to  arteriosclerosis. 

The  chief  irregularities  are  (1)  auricular  flutter,  (2) 
auricular  fibrillation,  (3)  ventricular  fibrillation,  (4)  au- 
ricular extrasy stole,  (5)  ventricular  extrasystole,  (6)  heart 
block,  partial  or  complete. 

Auricular  Flutter 

Auricular  flutter  is  an  abnormal  rhythm  characterized  by 
very  rapid,  but  rhythmic  auricular  contractions  usually  250 
to  300  per  minute.  The  auricular  contractions  are  so  rapid 
that  the  ventricle  can  not  respond,  so  that  an  electrocar- 

131 


132 


AT1TKHI()S('I.E1U)SIS 


(lia^'rain  of  a  licart  in  siicli  a  stato  (Fi^'.  40)  sliow.s  tlio 
ventricle  ])eatiiii>'  re^i^'ularly  ])ut  at  a  iiiucli  slower  rate  than 
the  auricle. 

The  majority  of  cases  exhibiting  this  jjeculiar  rhythm  are 
over  40  years  of  age.    In  many  cases  sclerosis  of  the  coro- 


I.ead   II    (auricular   flutter). 


Lead  III    (auricular  flutter). 
Fig.    -40.— (After    Hart.) 

nary  arteries  as  a  part  of  general  arteriosclerosis  has  been 
found.  Auricular  flutter  can  be  suspected  when  the  pulse 
is  regular  or  not  particularly  irregular  and  a  fluttering, 
rapid  pulsation  is  seen  in  the  jugular  vein  on  the  right  side. 
One  can  only  be  sure  of  the  condition  by  making  graphic 
records  of  the  heart. 


IMPORTANT    CAKDIAC    IRREGULARITIES  133 

Attacks  usually  come  on  suddenly  and  may  disappear  as 
suddenly,  suggesting  paroxysmal  tachycardia.  The  patient 
feels  a  commotion  in  his  chest,  dyspnea,  precordial  distress, 
etc.  The  attack  may  last  for  weeks  or  months,  in  which 
case  the  patient  may  carry  on  his  usual  work  but  l)e  con- 
scious of  palpitation  in  his  chest.  One  may  safely  assume 
that  the  flutter  is  a  sign  of  a  failing  myocardium  and  sooner 
or  later  the  heart  will  pass  to  the  graver  stage  of  auricular 
fibrillation. 

Auricular  Fibrillation 

In  this  condition  the  auricle  is  widely  dilated  and  over  its 
surface  are  countless  twitchings  of  individual  muscles  giv- 
ing to  the  auricle  the  appearance  of  a  squirming  bunch  of 
worms.  Such  a  condition  may  be  readily  produced  in  a 
dog's  exposed  heart  by  direct  faradization  of  the  auricle. 
It  should  be  seen  by  every  physician  in  order  fully  to  ap- 
preciate the  passive,  dilated  sac  part  which  the  auricle 
plays  when  in  such  a  state.  There  is  no  auricular  wave  on 
the  electrocardiogram  (Figs.  41  and  42)  only  a  series  of  fine 
tremulous  lines,  and  the  ventricles  beat  irregularly  with 
many  dropped  beats  and  variations  in  the  size  and  force  of 
individual  l)eats.  Extrasystoles  are  also  frequent.  The  heart 
is  a])solutely  irregular.  Such  a  condition  is  readily  recog- 
nizable as  the  state  of  broken  compensation.  Graphic  rec- 
ords are  not  essential  as  in  auricular  flutter  to  establish 
the  condition.  Inspection  of  the  root  of  the  neck  for  jugular 
pulsations  and  examination  of  the  pulse  with  the  patient's 
evident  dyspneic,  cyanotic,  edematous  condition  settles  the 
diagnosis. 

In  no  case  of  auricular  fibrillation  is  the  heart  muscle 
free  from  extensive  fibrous  changes.  These  may  be  the  re- 
sult of  general  arteriosclerotic  changes  or  may  result  from 
toxic  changes.  It  is  the  general  consensus  of  opinion  that 
auricular  fibrillation  may  persist  for  months  or  even  years. 
Some  hold  that  the  state  of  perpetual  irregular  jiulse  is 
associated  with  auricular  fibrillation.    If  that  is  true,  then 


134 


ARTERIOSCLEROSIS 


t  4  A  i 


f^Smmt^m0^ 


f-^V^^A^*. 


Fig.    41. — Electrocardiogram    .showing    auricular    fibrillation    in    T.eads    I     (ui)i)er)     and    II 
(middle   and    lower).      (Courtesy   of   Dr.    G.    C.    Robinson.) 


Fig.    42. — Auricular    librillation.      (After    Hart.) 


IMPORTANT    CARDIAC    IRREGULARITIES 


135 


auricular  fibrillation  may  last  for  many  years.  Patients 
may  go  about  their  work  but  always  live  with  the  imminent 
danger  of  a  sudden  dilatation  of  the  ventricle  and  symp- 
toms of  acute  cardiac  decompensation. 

In  these  cases  the  blood  pressure  is  of  particular  interest. 
It  is  often  stated  that  the  blood  pressure  is  lowered  as  com- 
pensation returns  and  digitalis  has  exhibited  its  full  action. 
As  a  matter  of  fact  this  statement  needs  some  modification. 
If  one  takes  the  highest  pressure  at  the  strongest  beat, 
which  may  be  only  one  in  a  dozen  or  more,  that  may  be  true, 
but  that  does  not  represent  the  action  of  the  nmcli  em- 


Op 

Nor. 
5      SU         27         m        29        80        Ul           1           2            »           4           5            6           7           3 

130  »-E^ 

120    " 

no:: 

100  __ 

ooi 

80^ 

1                 ^  >                                                                                                                                                        J 

^^■^^Bk 

^^^^^^HiHaiLflBL 

^^^^^^^^^^^^^H 

^^^^^^^^^^^^^^^^^ft 

^^^^^^^^^^^^^^^^^^^^^^ 

^^^^^^I^^^^^^^^^^^BH^ft.  «        Mm  ^ 

^^^^^^^^^^^^BBK^^^^B^^^  1  ^^VL  -flk^ 

^^^Hi^^S^Milb^S^J^MJHr  1  I^^^Bk.             .flLiafl 

70 

idoT       iiil      .mib<riiiiiiiiiiiiiiiiii.:L  _.^^i 

60      4- 

1    v^v    ^v 

r    ir^         l^m 

___±^Tri.. .  .TWt ±.. 

-DIGtTALIS" 

0336tt066666o;l8i) 

BU.  p.  8T3.1 

65     160                    IGO        162        ISO                    loi       118 

Fig.  43. — The  shaded  area  represents  the  pulse  delieit;  the  upper  edge  is  the  apex 
late,  the  lower  edge  the  radial  rate.  The  broken  line  indicates  the  "average  systolic 
blood  jiressure."  (Compare  these  values  with  the  figures  at  the  bottom  of  the  chart, 
which   show   the   systolic   blood   i)ressure   determined   by   the   usual   method.)       (After   Hart.) 

barrassed  heart.  We  know  that  the  circulation  is  much  in- 
terfered with,  that  there  is  hypostatic  congestion,  that  the 
mass  action  is  slow.  The  pulse  pressure  is  greatly  dis- 
turbed and  the  head  of  pressure  which  should  force  the 
blood  to  the  periphery  is  so  little  that  the  circulation  almost 
ceases. 

A  count  of  the  cardiac  contractions  heard  with  the  steth- 
oscope and  a  count  of  the  pulse  shows  a  great  discre])ancy 
in  number.  This  has  been  called  the  ''pulse  deficit"  (Hart). 
In  order  to  arrive  at  the  true  average  systolic  ])resaure  the 
following  procedure  is  done.     ''The  apex  and  radial  are 


136  AUTEUIOSCLEROSIS 

counted  for  one  minute,  at  the  same  time  by  two  observers, 
(if  possil)le)  then  a  bhiod  jiressure  cuff  is  applied  to  the 
arm,  and  the  pressure  raised  until  the  radial  pulse  is  com- 
pletely obliterated;  the  pressure  is  then  lowered  10  mm,, 
and  a  second  radial  count  is  made;  this  count  is  repeated 
at  intervals  of  10  mm.  lowered  pressure  until  the  cuff -pres- 
sure is  insufficient  to  cut  off  any  of  the  radial  waves  (be- 
tween each  estimation  the  pressure  on  the  arm  should  be 
lowered  to  zero).  From  the  figures  thus  obtained  the 
average  systolic  blood  pressure  is  calculated  by  multiplying 
the  number  of  radial  beats  by  the  pressures  under  which 
they  came  through,  adding  together  these  products  and 
dividing  their  sum  by  the  number  of  apex-beats  per  minute, 
the  resulting  figure  is  what  we  have  called  the  'average 
systolic  l)lood  pressure.'  "     (Fig.  43.) 


For  example 

:  "B.  S., 

April 

29,  1910,  Apex 

131;  radial,  101;  deficit,  30, 

BRACHIAL   PRESSURE 

RADIAL     COUNT 

100   mm. 

Hg. 

0 

90    iTim. 

13 

13x90  =  1170 

80    mm. 

47  -  13  = 

.34  X  80  =  2720 

70    mm. 

75  -  47  = 

28  X  70  =  19fi0 

60   mm. 

82  -  75  = 

7x60=    420 

50   mm. 

101-82  = 
Average 

19  X  50  =    950 
Apex  =  131)  7220 
systolic  l)lood-pressure  55   ] 

plus 
11   S.,  May   11,   1910,  Apex  79;    radial,   72;    deficit  7. 

BRACHIAL  PRESSURE      RADIAL  COUNT 

120  mm.  Hg.  0 

110    mm.  41  -14x110  =  4840 

100    mm.  64-44  =  20x100  =  2000 

90  mm.  72  -  64  =    8  x    90  =    720 

Apex  =  79)  7560 
Average   systolic  blood-pressure   95   jilus" 

The  diastolic  pressure  in  these  cases  can  not  be  deter- 
mined except  approximately.  This  may  be  done  by  using 
an  instrument  with  a  dial  and  noting  the  pressure  wdiere 
the  oscillations  of  the  dial  hand  show  the  maximum  excur- 
sion. The  diastolic  pressure  is  not  at  all  important  under 
such  conditions  of  acute  cardiac  breakdown.  It  would 
make  no  difference  in  treatment  whether  the  case  was  one 


IMPORTANT    CAPiDIAC    IPPEGULARITIES 


137 


138  ARTERIOSCLEROSIS 

of  pure  cardiac  disease  or  one  of  the  hypertension  groups. 
After  the  heart  has  rallied  and  the  circulation  is  reestab- 
lished, then  a  careful  determination  of  the  diastolic  pres- 
sure can  be  made  and  the  prognosis  will  rest  on  what  is 
found  at  the  compensated  stage. 

Ventricular  Fibrillation 

Ventricular  fibrillation  as  its  name  implies,  is  fibrillation 
of  the  ventricle  analogous  to  that  of  the  auricle,  but  the 
condition  is  rarely  observed  as  it  is  incompatible  with  life. 
It  has  been  shown  that  hearts  at  the  time  of  death  at  times 
enter  a  state  of  fibrillation  of  the  ventricles  and  that  cases 
of  sudden  death  may  be  due  to  this  condition.  Kecently 
G.  Canby  Robinson*  has  seen  and  made  electrocardiograms 
of  a  case  of  ventricular  fibrillation.  (Fig.  44.)  The  case 
was  that  of  a  woman  forty-five  years  old,  'Svlio  had  a  se- 
ries of  attacks  of  prolonged  cardiac  syncope,  closely  re- 
sembling Stokes-Adams  syndrome,  from  which  she  recov- 
ered. ' '  During  an  attack  of  unconsciousness  in  which  there 
was  no  apex  beat  for  about  four  minutes,  the  electrocardio- 
gram was  taken.  Following  this  the  tracings  showed  an 
almost  regular  heart  beating  at  the  rate  of  85  to  100  per 
minute.  The  patient  had  three  convulsions  and  died  with 
edema  of  lungs  about  30  hours  after  the  attack  of  ventricu- 
lar fibrillation. 

Autopsy  revealed  chronic  fibrous  endocarditis  of  aortic 
and  mitral  valves,  arteriosclerosis,  bilateral  carcinoma  of 
the  ovaries,  and  signs  of  general  chronic  passive  congestion. 

It  is  possible  that  the  syncopal  attacks  in  this  case  were 
the  result  of  sclerosis  of  the  vessels  supplying  the  heart 
muscle  although  careful  microscopical  examination  did  not 
throw  much  light  on  the  ultimate  cause. 

Extrasystole 

Whenever  there  is  a  dropped  beat  or  an  intermittent  pulse 
one  may  l)e  sure  that  it  is  the  result  of  an  extrasystole. 


'Robinson,  G.   C,  and  Bredeck,  J.  F.:     Arch.  Int.  Med.,   1917,  xx,  725. 


IMPORTANT    CARDIAC    IRREGULARITIES 


139 


Such  extrasystoles  are  i^roduced  in  tlie  ventricle  at  some 
point  otlier  tliaii  tlie  regular  path  of  conduction  of  impulises. 
The  extrasvbtole  may  have  its  origin  in  either  the  auricle 
or  the  ventricle.  If  there  is  auricular  extrasystole  it  can 
not  usually  be  recognized  except  by  graphic  methods.  (Fig. 
45.)  The  ventricular  extrasystole  on  the  contrary  is  com- 
monlv  seen  and  readilv  recoiiiiized.    ]\[ost  of  those  seen  in 


Fig.    45. — I'Mectrocardiograin    showing   auricular   extrasystoles    (P).    Courtesy   of   Dr.    G.    C. 

Robinson.) 


Fig.  4fi. — Electrocardiogram  showing  ventricular  extrasystole.  Heart  rate  56-60 
beats  per  minute.  Note  that  diastolic  iiause  in  which  extrasystole  occurs  is  practically 
equal    to    two    normal    diastolic   pauses.      (Courtesy    of    Dr.    G.    C.    Robinson.) 

the  clinic  have  their  origin  in  some  part  of  tlie  ventricular 
Avail.  Their  two  characteristics  are  that  they  occur  too 
early  and  that  they  are  followed  l)y  a  pause  longer  tlian  the 
normal  diastolic  pause.     (Fig.  4G.) 

AVhen  one  listens  over  the  chest  to  a  heart  when  extra- 
systoles are  occurring,  one  suddenly  hears  a  Aveak  beat 


140  AltTEllIOSCLEROSIS 

^^ilicll  lias  taken  place  rather  too  early  after  the  previous 
systole  to  he  strong  enough  to  effect  the  opening  of  the 
aortic  valves.  Consequently  there  is  no  pulse,  the  blood 
does  not  move,  and  that  heat  is  lost  to  the  circulation. 
Moreover,  when  the  next  regular  stinudus  conies  from  the 
s-a  node  it  finds  the  ventricle  in  a  refractory  condition, 
having  just  ceased  a  contraction,  and  it  is  not  until  the  next 
sinus  impulse  that  the  ventricle  responds  normally.  (Fig. 
46.) 

Patients  who  liave  occasional  extrasystoles  will  say  that 
all  of  a  sudden  the  heart  turns  upside  down  in  the  chest. 
Sometimes  there  is  slight  sliarp  twinge  of  pain.  Patients 
are  at  times  cpiite  alarmed  about  their  condition.  Provided 
there  is  no  evidence  of  gross  myocardial  lesion,  the  extra- 
systole  itself  is  of  no  great  significance. 

While  many  cases  showing  pathologic  causes  for  extra- 
systoles  have  more  or  less  marked  arteriosclerosis,  there 
are  other  states  in  which  no  arteriosclerosis  is  found  where 
the  extrasy stole  is  present. 

Heart  Block 

As  heart  block  occurs  frecpiently  in  cases  characterized 
by  extensive  arteriosclerosis,  a  brief  discussion  of  the  essen- 
tial features  Avill  be  given.  It  is,  however,  probable  that 
arteriosclerosis  is  not  the  cause  of  any  of  the  cases  of  heart 
block  directly,  but  it  is  only  a  result  of  the  same  etiological 
conditions  which  produce  the  lesion  or  lesions  which  result 
in  heart  block.  We  may  define  heart  block  as.  the  condi- 
tion in  which  the  auricles  and  ventricles  beat  independently 
of  each  other.  There  may  ])e  delayed  conduction  (P'ig.  47), 
partial  (Pig.  48),  or  complete  heart  block  (Fig.  49).  In 
the  former  there  are  ventricular  silences,  during  Avliich  the 
auricles  beat  two,  three,  four,  five,  even  up  to  nine  times, 
with  only  one  ventricular  conti'action.  It  is  l)elieved  by 
most  physiologists  that  the  essential  factor  in  the  produc- 
tion of  heart  block  is  an  interference  in  the  conduction  of 


I.MPOUTAXT    CARDIAC    IRRECI'I.AUITIKS 


141 


impulses  from  tlic  auricles  to  the  veuti-icles  tlirouL;li  tlie 
band  of  tissue  kuown  as  the  aurieuloveiitrieular  ])undle. 
The  bundle  of  nmseles  described  by  ]Lis  in  1905,  con- 


I'ii:  4/. —  I'.lectrocardiugrani  showing  delayed  conduction  (lengthening  of  I'-R  inter- 
val). These  P-R  intervals  are  quite  regular.  When  irregular  there  is  apt  to  be  extra- 
systole  of  ventricle  or  occasional  blocking  of  imi)ulse  going  to  ventricle.  (Courtesy  of 
l')r.    G.    C.    Koliinson.) 


15*-  Uo.4 


o.ioo  o.xJT 


Fig.  48. — Electrocardiogram  showing  partial  heart-block  in  the  three  leads.  Note 
the  variability  of  P-R  interval  calculated  in  seconds  in  Lead  II.  (Courtesy  of  Dr. 
G.    C.    Robinson.) 

nectiug  the  auricles  and  ventricles,  has  been  definitely 
shown  to  be  the  path  through  Avhich  imjiulses  having  their 
origin  in  the  orifices  of  the  great  veins  pass  to  the  ventri- 


142 


AirrKiMosci.Kr.osrs 


cles,     Tlio  situation  and  size  oC  tliis  binidlc  lias  boeri  tliiis 
described  in  man  by  Iletzer: 

"AVlieii  viewed  from  tlie  left  side,  tlie  bundle  lies  just 
above  the  nuiseular  septum  of  the  ventricles  and  below  the 
membranous  seijtum.  In  some  hearts  the  muscular  septum 
is  so  well  developed  that  it  enveloi)s  the  bundle.  It  is  then 
diflficult  to  find,  but  occasionally  it  can  ])e  seen  directly 
by  means  of  transmitted  light.    From  the  left  side  the  bun- 


515  .55'?  .S5X  .517 


,SHc  SH>  .5' if 


.SH-l  .THI 


Fig.    49. — Com])lete   heart    ijlock.      (Courtesy   of    Dr.    G.    C.    Kobinson.) 

die  can  be  followed  no  farther  posteriorly  than  the  right 
tibrons  trigone,  for  here  the  connective  tissue  becomes  so 
dense  that  it  is  diflficnlt  to  dissect  it  away.  The  impression 
is,  therefore,  received  that  this  mass  of  connective  tissue 
forms  the  insertion  of  the  bundle.  The  bundle  may  be  fol- 
lowed anteriorly  nntil  it  becomes  intimately  mixed  with  the 
musculature  of  the  ventricles. 


IMPORTANT   CARDIAC    IRREGULARITIES  143 

"AVlieii  viewed  from  tlie  ri^iit  side  of  the  lieart,  the 
bundle  can  not  be  seen,  because  it  is  covered  l)y  tlie  mesial 
leaflet  of  the  tricuspid  valve,  whose  line  of  attachment 
passes  obliquely  over  the  membranous  septum.  Then,  if 
the  endocardium  is  removed  from  the  jiosterior  part  of  the 
septum  of  the  auricle  up  to  the  membranous  septum,  the 
posterior  part  of  the  auriculoventricular  bundle  will  be  ex- 
posed. If,  in  addition,  the  membranous  septum  be  removed, 
the  bundle  may  be  traced  from  the  point  to  which  it  could 
be  followed  when  viewed  from  the  left  side  as  it  passes 
posteriorly  over  the  muscular  septum.  In  the  region  of  the 
auriculoventricular  junction  it  loses  its  compactness,  the 
fibers  divide,  and  the  bundle  seems  to  fork.  One  branch 
passes  into  the  superficial  part  of  the  valve  musculature 
which  descends  from  the  auricles,  and  the  other  branch 
passes  directly  into  the  musculature  of  the  auricle. 

*' Briefly,  the  auriculoventricular  bundle  runs  posteriorly 
in  the  septum  of  the  ventricles  about  10  mm.  below  the 
posterior  leaflet  of  the  aortic  semilunar  valves ;  with  a  gen- 
tle curve  it  passes  posteriorly  just  over  the  upper  edge  of 
the  muscular  septum  and  sends  its  fibers  into  the  muscula- 
ture of  the  right  auricle  and  of  the  auricular  valves.  In 
the  heart  of  the  adult  the  bundle  is  18  nnn.  long,  2.5  mm. 
wide,  and  1.5  mm.  thick."     (Erlanger.) 

All  normal  impulses  have  their  origin  in  the  sino-auric- 
ular  node  at  the  junction  of  the  superior  vena  cava  with 
the  right  auricle  (Fig.  50).  From  there  the  imi)ulse  travels 
in  the  wall  of  the  auricle  in  the  interauricular  septum  to  the 
node  of  Tawara  or  A-V  node  (Fig.  51),  thence  through  the 
bundle  of  His  to  be  distributed  to  the  fibers  of  the  right  and 
left  ventricles.  This  secpience  is  orderly  and  perfectly 
regular. 

It  has  also  been  shown  that  the  independent  auricular 
and  ventricular  rates  vaiy  somewhat,  that  of  the  auricle 
being  in  general  faster  than  that  of  the  ventricle.  A  strip 
of  mammalian   ventricle   placed   outside   of   the   body   in 


144 


AIITKRTOSCT.KTIOSIS 


])ro])er  siin'ouii(liiigs  will  l)('<>iii  to  boat  autoiiiatieally  at 
the  rate  of  ahoiit  40  boats  a  iniiiute.  Expcriiiioiitally  various 
grades  of  lieart  block  bave  been  produced   in  the  dog's 


Fig.    50. — Showing   alternating    i)eriods    of    sinus    rhythm    and    auricuUjventricular    rhythm. 
(After  Eystcr  and   Kvans.) 


rrrrrrrrrrrrrrrrrT' 


MKk^tkMKkMKkJtKmJKKmMKk  flBuHU^LMUM  flB  i^fc^^fc^^fc^^R.^^.^^i^^^^^ 


'^«'***s«*i^^'^. 


Fig.    .Si. — Period    of   aiiriculoventricular   or   "nodal"    rhythm    following   exercise    in    sitting 
posture.      (After   Eyster   and    Fvans.) 


Fig.    52. --Influence    of    mechanical    pressure    on    the    right    vagus    nerve.       (After    Ivyster 

and    Kvans.) 

lieart  by  more  or  less  compression  of  the  l)undle  at  the  A-V 
ring,  Tlie  block  may  be  partial,  wlien  two  to  nine  auricular 
beats  occur  to  every  one  of  the  ventricle,  up  to  absolute 


IMPORTANT    CARDIAC    IRREGULARITIES 


145 


Fig.    53. — Schematic  distriljiitioii   of   right   and   left  vagus.      (After    Hart.) 


complete  block  when  the  auricles  and  ventricles  beat  inde- 
pendently of  one  another. 

In  any  stage  of  partial  block,  pressure  on  the  vagus  nerve 


146  ArvTErjOSOLEROSIS 

ill  tlic  neck  ])r()(lii('Os  ('crlaiii  spocifK'  cliang'os.  (Fig.  52.)- 
Robiusoii  and  Di-apor*  liavc  foiiiid  (jualitativc  difforoiicos 
in  tlic  two  vagi.  The  rigid  vagus  sends  most  of  its  fillers  to 
the  s-a  node  (Fig.  oo)  and  lias  a  more  evident  influence  on 
the  rate  and  force  of  the  cardiac  contractions.  The  major- 
ity of  fibers  from  the  hd't  vagus  are  distril)uted  to  the  A-V 
node  so  that  its  most  evident  action  is  upon  the  conductiv- 
ity of  the  impulse.  Pressure  then  on  the  right  vagus  will 
have  a  tendency  to  slow  the  whole  heart.  Pressure  on  the 
left  vagus  Avill  have  a  tendency  to  prolong  the  P-R  interval 
until  even  complete  block  occurs.  Even  when  the  heart 
block  is  complete,  stimulation  of  the  accelerator  nerve,  as  a 
rule,  increases  the  rate  of  both  auricles  and  ventricles. 

If  the  block  is  functional,  depending  upon  some  tempo- 
rary overstimulation  of  the  vagus  nerve,  atropin,  Avhicli 
paralyzes  the  endings  of  the  vagus,  will  naturally  lift  the 
block.  If  the  lilock  is  due  to  some  actual  lesion  of  the  bun- 
dle of  His,  such  as  fibrosis,  gumma,  or  other  lesion,  then 
atropin  will  have  no  influence  to  terminate  the  block.  In 
this  manner  we  are  able  to  distinguish  between  functional 
and  oro-anic  heart  block. 


*Jour.    Kxper.    Med.,   1911,  xiv,  217. 


CHAPTER  V 

BLOOD  PRESSURE  IN  ITS  CLINICAL  APPLICATIONS 

It  is  well  to  bear  constantly  in  mind  the  point  made  over 
and  over  in  tliis  work,  that  l)lood  jiressnre  is  only  one  of 
many  methods  of  acquirino-  information.  He  who  worships 
his  sphysniomanometer  as  a  thing  apart  and  infallil)le  will 
sooner  or  later  come  to  grief.  Judgment  nnist  he  used  in 
interjireting  changes  in  blood  pressure  just  as  judgment  is 
essential  in  properly  evaluating  any  instrumental  help  in 
diagnosis.  One  must  not  forget  the  personal  equation 
which  enters  into  even  accurate  instrumental  recording  in 
medicine  and  surgery. 

In  this  chapter  there  will  l)e  no  attempt  to  quote  largely 
from  what  others  have  said  or  thought.  Every  one  has 
his  own  opinion  as  to  the  value  of  certain  methods  after  he 
has  worked  with  them  for  a  long  time.  The  ideas  here  ex- 
pressed, excejjt  in  cases  where  no  opportunity  has  offered 
to  make  personal  studies,  are  those  gathered  from  personal 
experience. 

Blood  Pressure  in  Surgery 

Careful  estimation  of  the  blood  pressure  in  surgical  cases 
has,  at  times,  great  value.  In  all  surgical  diseases  the  most 
important  fact  to  know  is  not  the  systolic  pressure,  but  the 
pulse  pressure.  If  the  pulse  pressure  keeps  within  the 
range  of  normal,  does  not  drop  much  below  30  nun.  in  an 
adult,  then  so  far  as  we  can  tell  the  circulation  is  being 
carried  on.  When  the  systolic  pressure  is  gradually  fall- 
ing and  the  diastolic  remains  the  same,  the  circulation  is 
failing  and  unless  the  pulse  pressure  can  be  established 
again  the  patient  will  die.  Again  we  see  the  value  of  the 
pulse  pressure. 

147 


]  48  ArtTERIOSCLEFiOSlS 

All  ])1'()1oh^(h1  f(>l)ril('  diseases  tond  to  prodiico  a  lowoi'infi; 
of  the  ))1()()(1  pressure  picture.  Tlie  diastolic  does  not  fall  to 
the  same  extent  as  the  systolic  so  that  there  is  a  pulse  pres- 
sure smaller  than  normal.  This  is  to  he  expected  from  what 
\\o,  know  of  the  general  depression  of  the  circulation  in 
fev(!rs.  The  hlood  pressure  reading  is  only  a  graphic  rec- 
ord of  what  we  have  long  known,  and  ena])les  us  from  day 
to  day  accnrat(dy  to  measure  tlie  general  circulation. 

Head  Injuries 

It  was  claimed  that  in  fracture  of  the  skull  or  in  con- 
cussion much  could  be  gained  by  freciuent  estimations  of 
tlie  blood  pressure.  Tliis  seemed  i)robal)le  in  the  light  of 
experiments  on  compressing  the  brains  of  dogs  by  the  use 
of  bags  inserted  through  trei)hine  openings  (Cushing).  In 
the  clinic,  however,  it  has  not  been  found  of  any  material 
value.  It  has  a  value  in  differentiating  a  simple  fracture, 
let  us  say,  from  a  case  of  uremia  which  is  picked  up  on  the 
street  with  a  bump  on  the  head.  There  the  high  pressure 
usually  found  would  at  once  direct  attention  to  the  kidneys 
and  the  newer  methods  of  blood  examination  would  at  once 
settle  the  question.  Naturally  uremics  may  also  have  skull 
fracture.  There  the  diagnosis  would  be  complicated.  A 
decompression  done  at  once  would  be  indicated.  If  the 
skull  fracture  happened  in  a  uremic,  the  decompression 
would  probably  do  no  harm.  In  fact,  there  are  some  who 
advise  decompression  for  uremia. 

Shock  and  Hemorrhage 

In  shock  the  ])lood  pressure  picture  is  low  but  the  pulse 
pressure  drops  to  al)normally  low  figures.  It  seems  to  me 
that  the  blood  pressure  instrument  has  its  greatest  value 
in  surgery  in  the  warning  it  gives  to  the  operating  surgeon 
in  cases  of  impending  shock. 

It  is  well  known  that  the  first  effect  of  ether,  the  com- 


BLOOD    PRESSURE 


149 


HOSPITAL   /I  J  (^Jf^AMti. E  E  JjO OjiTy  _ 
N0.^X?A1L_ 

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DRAINS 

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CULTURES.. 


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REMARKS- 


Fig.  54. — Blood  pressure  record  from  a  normal  reaction  to  ether.  Note  that  the 
systolic  and  diastolic  rise  and  fall  together.  At  the  end  of  the  anesthetization  the  pulse 
pressure  is  practically  the  same  as  at  the  beginning.  Compare  this  with  the  record  in 
Fig.    55,  where  the  operation   had   to  be  discontinued  on  account   of  the  onset   of   shock. 


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sPEciMEN.GooeYtJkx  .^u4\»  $(TOm  o\iaru - 

DRAINS \^ .^ 

CULTURES ,.. 

CLOSURE..  ANAESTHETIST-.^Jr".     t'^Q'  

REMARKS  ~^«^\tcK>on  ^V\aN\o\iO  av»a  toawi.  .  Qc»\\  VWiUr  ^y\A  Ao  Vit  ^i>\ci  .tOi^Vu .  aa^r  ftVanea 
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— !fCwo*cA--e?<'^(4  -^ime^ ' , /_ 

Fig.  .S.i. —  Ik'Kiiining  of  operative  .sliock.  Cliart  showing  the  method  of  recording  blood  ])res- 
siire    during    oi)eration. 

Note  that  the  imlse  and  respiration  show  no  remarkable  changes,  but  the  blood  pressure 
steadily  fell,  the  systolic  more  than  the  diastolic  so  that  the  iiulse  pressure  was  gradually  reaching 
the  danger  point.  Further  work  on  this  case  was  stopjied  following  the  warning  given  by  the 
blood  pressure.  The  patient  was  returned  to  the  ward  and  a  week  later  anesthesia  was  again 
given,   the   operation   was  completed,   and   the   jiatient   had   a   satisfactory   convalescence. 


BLOOD   PEESSURE 


151 


monly  used  anestlietie,  is  to  raise  tlie  ])lood  pressure  and 
quicken  tlie  pulse  rate.  Tlie  whole  blood  pressure  picture 
is  at  first  elevated  (Fig.  54).  Soon  the  whole  pressure  falls 
slightly  but  continues  at  a  higher  level  than  normal.  The 
diastolic  pressure  drops  back  neai'ly  to  normal  and  the  in- 
creased pulse  pressure  is  due  almost  entirely  to  the  slight 
rise  in  the  systolic  pressure.  Now  the  whole  duty  of  the  an- 
esthetist is  to  administer  the  ether  so  that  this  ratio  of  sys- 
tolic and  diastolic  is  maintained  throughout  the  operation. 


■ 

1 

M^ 

■Mi 

^Bm^^^^^^^^H^^BHH^^r    K    ^^^^H^^^^^^^^^^MaHi^^^^^^^^^^^^^^^^^^^B 

Fig.  56. — Showing  method  of  using  blood  pressure  instrument  during  operation  with- 
out interfering  with  the  operator  or  assistants.  Sheet  thrown  baci<  to  show  cuff  on 
arm  of  i)atient.  Anesthetist  has  chart  on  table  beside  him,  dial  pinned  to  pad  in  full 
view,   bulb   near   hand,      lixtra  tubing  must  be   put   on   the   blood   pressure   instriniient. 

Warning  comes  to  him  of  impending  shock  before  it  comes 
to  any  one  in  the  neighborhood  (Fig.  55).  Any  sudden 
change  in  the  pressure  is  a  signal  for  increased  watchful- 
ness. Should  the  pressure  all  at  once  drop  he  can  innne- 
diateh^  notify  the  surgeon  and  institute  measures  to  resus- 
citate the  patient. 

A  method  which  is  widely  used  is  as  follows:  The  anes- 
thetist wraps  tlie  cuff  of  one  of  the  dial  instrnments  around 
the  patient's  arm,  and  arranges  the  dial  so  that  it  can  easily 


1 52  ARTERIOSCLEROSIS 

be  seen  ])y  him  at  all  times.  This  does  not  in  any  way  inter- 
fere witli  the  work  of  the  sur<:!,eon.  Over  the  l)rachial  ar- 
tery below  the  cuff  is  the  bell  of  a  l)inaiiral  stethoscope  held 
in  place  by  the  strap  attachment  now  on  the  market.  The 
tul)es  of  tlie  stethoscope  are  long  enough  to  reach  conven- 
iently to  the  ear  ineces.  A  watch  is  pinned  to  the  sheet  of 
the  table.  He  has  a  chart,  as  illustrated  (Fig.  56)  on  a 
board  and  makes  a  dot  in  every  space  for  five  minute  inter- 
vals. By  joining  the  lines  a  curve  is  obtained  which  tells 
at  a  glance  what  the  circulation  is  doing.  I  feel  sure  that 
more  attention  and  care  exercised  on  the  iDart  of  the  anes- 
thetist would  be  the  means  of  conserving  many  lives  lost 
from  shock  following  operation. 

A  sudden  drop  in  the  pressure  picture  may  mean  a  large 
hemorrhage.  The  gradual  return  of  the  pressure  picture 
means  that  the  vasomotor  mechanism  has  acted  to  keep  up 
the  pulse  pressure.  Should  the  diastolic  pressure  contin- 
ually fall,  it  may  mean  that  the  hemorrhage  is  still  taking 
place  ( Wiggers ) . 

Blood  Pressure  in  Obstetrics 

One  might  affirm  almost  without  fear  of  contradiction 
that  the  constant  determination  of  blood  pressure  during 
pregnancy  is  more  important  than  the  examination  of  the 
urine.  Within  recent  years  a  number  of  observers  having 
access  to  a  large  material,  have  given  the  results  of  their 
findings.  There  is  a  striking  unanimity  of  opinion,  al- 
though now  and  then  a  difference  in  minor  details. 

The  blood  pressure  should  be  taken  frequently  during 
pregnancy.  The  usual  and  liighly  essential  precautions  in 
taking  pressure  in  general  ai)p]y  most  particularly  in  these 
cases.  Towards  the  end  of  pregnancy  the  pressure  should 
if  possible  be  taken  daily  and  oftener  if  necessary. 

Pressure  in  women  is  usually  below  120  mm.  Many  pa- 
tients have  a  temporary  rise  in  blood  pressure  during  preg- 
nancy, due  oftenest  to  constipation,  without  developing 


BLOOD    PRESSURE  153 

other  symptoms.  This  is  common  to  all  conditions  and  lias 
no  significance.  Some  think  that  an  abnormally  h)w  pres- 
sure, that  is,  a  systolic  below  90  mm.,  suggests  that  the 
patient  is  likely  to  react  nndnly  to  the  strain  of  labor.  This 
is  denied  by  others.  Among  1000  cases  (Irving)  the  pres- 
sure was  below  90  in  only  one  case.  A  gradually  rising 
pressure  precedes  albuminuria,  as  a  rule.  If  there  is  al- 
bumin without  change  in  i)ressure  the  albumin  may  usually 
be  disregarded.  Some  think  that  a  pressure  over  130  mm. 
systolic  should  be  carefully  watched.  The  danger  limit 
is  set  by  some  at  150  mm.  If  the  blood  pressure  from  the 
very  first  is  high,  it  may  mean  only  that  that  was  the  pa- 
tient's normal  pressure.  This  calls  for  increased  watchful- 
ness. It  is  held  by  some  that  high  blood  pressure  favors 
hemorrhage  and  probably  explains  the  hemorrhagic  lesions 
in  the  placenta  and  some  viscera  in  eclampsia  and  albumi- 
nuria. 

All  are  agreed  that  the  most  significant  change  is  the 
gradual  but  sure  rise  from  a  low  pressure.  AVlien  this  is 
combined  with  albuminuria  the  danger  of  toxemia  is  im- 
minent. The  high  blood  pressure  in  those  under  thirty 
years  of  age  seems  to  be  a  more  certain  sign  of  approach- 
ing toxemia  than  the  same  pressure  in  those  older.  The 
pressure  falls  within  a  few  days  to  its  normal  after  delivery 
in  the  toxic  cases. 

Although  the  emesis  gravidarum  is  held  to  be  a  sign  of 
a  toxemia  of  some  unknown  nature,  the  l)lood  pressure  is 
never  raised  even  in  the  pernicious  form. 

Infectious  Diseases 

In  all  infectious  diseases  the  ])lood  pressure  tends  to  be 
lower  than  normal.  During  chills  the  systolic  may  rise  to 
great  height  due  to  the  violent  muscular  contractions. 

AVe  found  the  blood  pressure  of  great  value  in  giving 
information  concerning  the  circulation.    Again  we  repeat 


154  AKTEIUOSCLEROSIS 

that  it  is  not  tlie  systolic  alone  or  the  diastolic  alone  but  the 
pulse  pressure  which  we  wish  to  keep  informed  about.  In 
pneumonia  we  have  tried  out  Gibson's  law  only  to  discard 
it.  This  so-called  law  is  that  in  pneumonia  the  systolic 
pressure  in  millimeters  should  remain  above  the  figure  for 
the  pulse  rate.  When  the  figure  in  mm.  of  pressure  is 
equalled  by  or  exceeded  by  the  pulse  rate  the  prognosis  is 
grave. 

In  typhoid  fever  we  have  made  many  estimations  at  va- 
rious stages  of  the  disease.  We  can  only  say  that  the  pres- 
sure picture  tends  to  fall  during  the  course.  The  systolic 
falls  more  than  the  diastolic  so  that  it  is  not  uncommon 
to  see  pulse  pressures  of  20  mm.  at  the  beginning  of  con- 
valescence in  spite  of  the  high  caloric  feeding  practiced. 
At  the  time  of  i3erforation  the  systolic  pressure  may  be 
raised.  This  is  only  the  reflex  from  the  initial  pain.  Soon 
tlie  pressure  falls  and  if  peritonitis  sets  in,  the  pressure  is 
exceedingly  low  and  the  pulse  pressure  gradually  falls  un- 
til the  circulation  can  no  longer  be  carried  on.  In  large 
hemorrhage  the  pressure  suddenly  falls.  If  only  one  hem- 
orrhage has  occurred  a  gradual  rise  takes  place,  but  the 
general  pressure  picture  remains  at  a  lower  level  for  days, 
gradually  returning  where  it  M^as  before  the  hemorrhage. 

In  beginning  failure  of  the  circulation  we  found  ele- 
vation of  the  foot  of  the  bed  about  nine  inches  to  be  of  such 
value  that  w^e  felt  there  must  be  some  increase  in  blood  pres- 
sure. Numerous  readings  were  made  covering  a  period  of 
several  months.  Although  we  felt  certain  that  the  circula- 
tion was  improved,  we  rarely  needed  cardiac  stimulation, 
we  never  could  prove  any  increase  of  blood  pressure  with 
the  sphygmomanometer. 

In  all  infectious  diseases  there  is  no  help  offered  by  blood 
pressure  estimations  in  diagnosis.  The  sole  and  important 
use  is  that  of  keeping  track  of  the  circulation. 


BLOOD    PRESSURE  155 

Valvular  Heart  Disease 

No  rules  can  l)e  laid  down  for  l)lood  Tjressure  in  valvular 
heart  disease.  Aortic  stenosis,  the  rarest  of  the  valvular 
lesions,  is  practically  always  accompanied  hy  hi,2,h  pressure 
picture.  Mitral  stenosis  on  the  contrary  usually  shows  a 
low  pressure  picture.  Mitral  insufficiency  may  show  an 
exceedingly  low  picture  or  an  exceedingly  high  picture. 
Aortic  insufficiency  also  may  he  accompanied  hy  a  high 
systolic  or  hy  a  normal  systolic  pi'essure.  It  depends  on  the 
etiology.  Practically  all  the  rheumatic  cases  have  low  pres- 
sure, the  syphilitic  cases  have  a  high  pressure.  It  is  char- 
acteristic of  all  cases  of  aortic  insufficiency  that  the  dias- 
tolic pressure  is  low,  even  as  low  as  30  mm.  The  pulse 
pressure  is  invariahly  liigh.  Usually  there  is  no  difficulty 
in  determining  the  diastolic  pressure.  The  intense  third 
tone  suddenly  hecomes  dull  at  the  point  of  diastolic  pres- 
sure and  frequently  the  dull  sound  can  he  distinctly  heard 
over  the  artery  down  to  the  zero  of  the  scale.  If  difficulty 
is  found  in  reading  the  diastolic  as  the  pressure  is  reduced, 
the  estimation  may  he  reversed  and  the  pressure  gradually 
increased  from  zero  to  the  point  where  the  dull  tone  sud- 
denly hecomes  loud  and  clear.  These  points  always  coin- 
cide. 

Kidney  Diseases 

This  has  already  ])een  discussed  somewhat  fully  in  Chap- 
ter III  and  will  receive  more  consideration  later.  It  might 
be  remarked  in  passing  that  in  a  case  of  seeming  coma 
Avhere  albumin  is  found  in  the  urine  l)ut  where  the  blood 
pressure  is  low  or  normal,  I  have  found  at  autopsy  in  sev- 
eral cases  pyonephrosis  and  not  chronic  nephritis.  The 
])lood  pressure  may  be  useful  in  differentiating  uremic  coma 
from  the  coma  of  pyonephrosis.  Also  in  the  cases  of  coma 
with  anasarca,  either  the  acute,  subacute  or  chronic  form 
the  blood  pressure  is  not  raised  as  a  rule.  Otliei*  diseases 
of  the  kidney,  as  tuberculosis,  cancer,  infection  with  pyo- 


156  ARTERIOSCLEROSIS 

geiiic  organisms,  are  not  accompanied  witli  any  notal)]e 
changes  in  blood  pressure. 

Other  Diseases,  Liver,  Spleen,  Abdomen,  etc. 

Blood  j)ressure  is  only  of  value  in  the  al)ove  diseases  in 
affording  information  concerning  the  state  of  tlie  circula- 
tion. Tliere  is  nothing  characteristic  about  the  pressure 
in  any  of  these  diseases. 


CHAPTER  VI 

ETIOLOCY 

The  causes  of  arteriosclerosis  are  many  and  varied.  No 
two  persons  liave  tlie  same  resisting  power  toward  poisons 
tliat  circulate  in  the  blood.  Some  go  through  life  exjDosed 
to  all  the  infectious  diseases  without  ever  becoming  in- 
fected, while  others  fall  easy  victims  to  every  disease  that 
comes,  no  matter  how  careful  they  may  be,  and  it  is  ciuite 
the  same  in  regard  to  the  resistance  of  the  arterial  tissues. 
If  tlie  tubing  is  of  tirst  class  quality  and  the  individual  does 
not  place  too  nuicli  strain  on  it,  he  may  live  to  the  biblical 
three-score  years  and  ten,  and  ])ossess  arteries  which  have 
undergone  such  slight  changes  that  they  are  not  palpable. 
Such  a  person  is,  however,  the  exception.  On  the  other 
hand,  if  the  tissue  is  of  poor  ciuality,  even  the  ordinary 
wear  and  tear  of  life  causes  early  changes  in  the  vessels, 
and  a  person  of  forty  may  have  hard  arteries. 

We  have  described  in  a  previous  chapter  the  changes 
which  normally  occur  in  the  arteries  as  age  advances.  An 
artery  that  is  normal  for  a  man  of  fifty  years  would  be 
distinctly  abnormal  for  a  boy  of  fifteen. 

Two  broad  divisions  of  arteriosclerosis  may  be  made: 
(1)  congenital,  or  the  result  of  inherited  tendency;  (2) 
acquired. 

Congenital  Form 

AVhen  Dr.  0.  AV.  Holmes  was  asked  how  to  live  to  the  age 
of  seventy,  he  replied  that  a  man  should  begin  to  pick  his 
ancestors  one  luuidred  years  before  lie  was  born.  Our 
parents  determine  the  character  of  the  tissues  with  which 
we  start  in  life,  and  this  determines  our  general  resistance. 
We  might   properly   speak   of   congenital    arteriosclerosis 

157 


158  ArvTEPJOSCLEPiOSlS 

wlicro  tlic  nrfoclcd  individual  liad  ])()()!■  arterial  tissue  Avitli 
wlncli  to  l)o<;iii  life,  for  that,  in  a  sense,  is  a  eong-eiiital  de- 
fect, and  arterial  tissue  tliat  is  poor  in  quality  is  prone  to 
disease. 

Tlie  author  is  nioi'e  and  more  impressed  Avitli  the  part  that 
heredity  plays  in  the  determination  of  arterial  degenera- 
tion. Especially  does  syphilis  in  tlie  parents  or  grand- 
parents leave  its  stigma  in  the  succeeding  generations  in 
the  shape  of  poor  arterial  tissue  which  is  prone  to  early 
degeneration.  Recently  AV.  W.  (Graves  has  called  atten- 
tion to  a  malformation  of  the  vertebral  border  of  the  scaj)- 
ula  which  consists  in  a  concavity  instead  of  the  normal 
convexity  of  the  bone.  To  this  malformation  he  has  given 
the  name,  scaphoid  scapula.  He  considers  this  to  be  but 
one  manifestation  of  a  general  lack  of  development  in  the 
individual.  He  speaks  of  this  maldevelopment  as  a  blight 
and  considers  that  syphilis  in  the  ancestors  is  responsible 
for  the  condition  in  the  offspring.  He  finds  that  even  in 
children,  the  subjects  of  the  scaphoid  scajDula,  the  arteries 
are  very  definitely  thickened.  AVhile  confirmation  of  his 
observations  is  lacking,  there  is  no  doubt  that  we  nmst  lay 
the  blame  for  much  of  the  arteriosclerosis  in  our  patients 
to  the  poor  quality  of  arterial  tissue  transmitted  by  an- 
cestors who  have  acquired  some  constitutional  disease.  It 
may  have  been  syphilis,  it  may  have  been  the  degeneration 
produced  by  alcohol  or  other  drug.  We  can  not  ignore  the 
part  which  heredity  plays.  The  various  factors  to  be  con- 
sidered in  the  production  of  the  acquired  form  of  arterio- 
sclerosis apx)ear  to  me  to  be  l)ut  contril)utory  factors  to 
a  very  great  extent,  the  essential  and  fundamental  factor 
being  the  quality  of  arterial  tissue  with  which  the  individ- 
ual is  endowed. 

Arteriosclerosis  may  occur  in  infants.  Cases  have  been 
reported  of  calcification  of  the  arteries  in  infants  and  chil- 
dren. The  arteriosclerosis  may  occur  without  nei3hritis  or 
rise  of  blood  pressure.     Cerebral  hemorrhage  in  a  child 


ETIOLOGY  159 

of  two  years  lias  Loeii  seen.  Heredity  in  these  cases  plays 
a  most  iinportaiit  role.  In  many  of  the  rei^orted  eases  there 
was  no  question  of  congenital  syphilis.  Aneurysms,  single 
or  multiple,  have  l)een  found  in  the  arteries  of  children, 
and  even  the  pulmonary  artery  may  show  sclerotic  changes. 

Acquired  Form 

As  a  rule  the  cases  usually  seen  helong  in  tiiis  group 
because  it  seems  as  if  a  connection  could  be  established  al- 
most always  between  one  or  more  of  the  etiologic  factors 
to  be  described  and  the  disease.  AVhile  this  ajiparently  is 
the  case,  we  must  never  lose  sight  of  the  part  which  the 
quality  of  the  tissue  plays.  When  we  leave  this  out  of  our 
calculations  we  undoul)tedly  make  many  false  deductions. 
When  two  men  of  the  same  age  who  have  been  exposed  to 
the  same  conditions  as  far  as  we  can  learn,  are  found  to 
have  quite  different  arteries,  the  one  normal,  tlie  other 
thickened,  we  must  postulate  congenitally  poor  tissue  on 
the  part  of  the  latter.  Such  tissue  readily  becomes  dis- 
eased following  conditions  which  would  very  likely  have 
produced  no  noticeable  effect  on  perfectly  normal,  healthy 
tissue.  ^_.         -^  X 

^^  Hypertension  ' 

Hypertension  must  still  be  reckoned  with  in  the  etiology 
of  arteriosclerosis  although  the  role  that  it  was  thought  to 
play  does  not  seem  so  important.  Changes  of  blood  pres- 
sure alone  are  not  considered  by  many  to  be  sufficient  for 
the  production  of  arteriosclerosis.  This  may  play  some 
part,  but  there  are  many  other  factors  mostly  unknown 
which  determine  in  any  case  the  production  of  arterial 
lesions.  i 

AVith  every  systole  of  the  heart,  blood  is  forced  out  into 
the  arterial  system  against  a  certain  amount  of  resistance 
represented  by  the  tonicity  of  the  capillary  area,  and  the 
amount  of  cohesion  between  the  viscous  blood  and  the  walls 


160  ArvTEPtTOSCLEROSIS 

of  llie  arlcriolcs.  AVlioii  a  dilatation  of  tlie  capillaries  over 
any  lar^e  area  tak'es  ])la('e,  the  blood  pressure  falls,  pro- 
vided tliei'e  ii^  no  eonijiensatory  conti'aetion  in  otlier  areas 
to  niak'e  up  for  tlie  decreased  resistance  in  tlie  dilated  ves- 
sels. The  viscosity  of  tlie  blood,  as  sucli,  jn'obaldy  lias 
very  little  effect  on  the  resistance  to  the  flow.  With  the 
systole  of  tiie  heart  there  is  a  sudden  dilatation  of  the  arch 
of  the  aorta,  and  a  wave  of  expansion  follows,  which  is 
transmitted  to  the  periphery  and  is  lost  only  in  the  capil- 
laries. 

The  blood  pressure  is  constantly  chang'inr?.  Physio- 
loft'ically  there  are  relatively  wide  variations  in  the  pres- 
sure in  a  perfectly  normal  individual.  There  are  some 
persons  who  have  hypotension,  a  blood  i)ressure  much  be- 
low the  normal.  Such  persons  have  nsually  small  hearts, 
small  aortas,  ami  they  seem  to  liave  l)ut  little  resistance 
to  disease.  ]\[any diseases,  especially  the  prolonged  fevers, 
diminish  markedly  the  blood  pressure.  AVliether  the  hyper- 
tension is  the  canse  of  the  structural  changes  that  are  found 
in  the  walls  of  the  vessels,  or  is  the  result  of  the  diminished 
area  of  the  arterial  tree  through  which  the  same  amount 
of  blood  has  to  ])e  driven  as  before  the  vessel  walls  became 
narrowed,  is  still  disputed.  As  has  been  stated,  experi- 
mental evidence  would  tend  to  place  the  initial  blame  upon 
the  poisons  circulating  in  the  blood,  which  first  damage  the 
vessel  walls.  The  subsecpient  changes  then  produce  thick- 
ening and  inelasticity.  Some  think  (Allbutt)  that  the 
hypertension  is  primary.  There  are  cases  seen  clinically 
that  lend  sujiport  to  this  view  and  there  is  experimental 
evidence  also  (v.  Chap.  II).  Not  infrequently  individuals 
in  middle  life  begin  to  show  increase  of  arterial  blood  pres- 
sure without  discoverable  cause.  In  such  case  it  may  be 
that  there  is  slowly  progressing  chronic  nephritis.  The 
urine  if  examined  only  superficially  in  single  specimens  may 
not  reveal  any  a])normaUties.  Careful  functional  examina- 
tion bv  means  of  the  newer  tests  mav  reveal  functional 


id  h'tii^f 


ETIOLOGY  161 

deficiency.  /  It  must  not  be  supposed  tliat  all  cases  of  in- 
creasing hypertension  are  cases  of  chronic  nephritis.  The 
opinion  lias  already  been  expressed  (Chap.  Ill)  concerning 
this  point.  Experience  has  convinced  me  that  the  opinion 
expressed  in  former  editions  is  not  altogether  correct. 

Age 

No  age  is  exempt  from  the  lesions  of  arteriosclerosis  if  we 
consider  the  two  groups.  However,  the  disease  is  seen  for 
the  most  part  in  persons  past  middle  life.  The  relative 
frequency  with  which  it  is  found  in  the  different  decades 
depends  on  so  many  factors  that  it  is  of  no  value  to  tabulate 
them.  As  has  been  stated,  arteriosclerosis  of  all  types  is 
an  involution  process  that  advances  with  age.  Longevity 
is  a  question  of  the  integrity  of  the  arterial  tissue,  and  no 
one  can  tell  what  sort  of  "vital  rubber"  (Osier)  any  one 
of  us  has.  However,  many  with  poor  tubing  may  make 
such  use  of  it  that  it  will  outlast  good  tubing  that  is  badly 
treated.  Unfortunately  we  have  no  way  of  telling  early 
enough  with  just  what  sort  of  arterial  tissue  we  are  start- 
ing life. 

Sex 

There  is  no  doubt  that  men  are  far  more  prone  to  arterial 
disease  than  women  are;  all  statistics  are  in  accord  on  this 
point.  This  is  explained  by  the  greater  exposure  of  men 
to  those  conditions  of  life  which  tend  to  produce  circulatory 
strain,  and  so  to  produce  arteriosclerosis,  or  vice  versa. 
Arteriosclerosis  in  women  is  not  often  seen  until  after  the 
fiftieth  year.  Cases  of  the  most  extreme  grade  of  pipe 
stem  arteries  are,  however,  seen  in  old  women,  and  calcified 
arteries  are  not  hard  to  find  among  the  inmates  of  an  old 
woman's  home. 

Race 

Some  of  the  most  beautiful  examples  of  arteriosclerosis 
in  this  country  are  seen  in  the  negro.     Not  only  is  this 


162  Ar/rERlOSCLEKOSTS 

disease  more  fi-(M{iieiit  in  the  l)la('k  race,  hut  tlie  a^-e  of  onset 
is  mueli  earlier  than  in  tlie  Caucasian.  Tlie  accidents  of 
arteriosclerosis,  viz.,  aneurysm,  cerehral  heniorrhaft'e,  etc., 
are  more  common  amonft-  the  nef>'ro  males.  The  etiologic 
factors  that  are  most  often  found  in  the  history  are  the 
jjrevalence  of  syphilis  and  hard  physical  lahor. 

Occupation 

Certain  occupations  have  a  distinct  causal  relationship  to 
arteriosclerosis;  among  such  are  particularly  those  entail- 
ing prolonged  muscular  exercise,  especially  if  nuich  lifting 
is  necessary.  Every  one  is  familiar  with  the  ijhenomena 
accompanying  the  exertion  of  lifting.  The  hreath  is  draA\'n 
in,  the  glottis  is  closed,  and  the  nuiscles  of  the  chest  wall 
are  lield  rigidly  while  the  exertion  lasts.  This  causes  a 
great  increase  in  l)lood  pressure,  and  constant  repetition 
of  this  will  produce  permanent  high  tension.  In  hospitals, 
the  stevedores  as  a  class  have  marked  arteriosclerosis,  and, 
almost  without  exception,  they  are  comparatively  young- 
men.  Occupations  that  are  accompanied  with  i)rolonged 
mental  strain,  such  as  now  occur  to  the  heads  of  large  man- 
ufacturing and  financial  institutions,  also  predispose  to 
early  arterial  changes.  Psychic  activity,  especially  when  it 
is  accompanied  by  worry,  is  a  potent  factor  in  the  produc- 
tion of  the  increased  l)lood  pressure  which  is  the  chief  factor 
in  producing  arterial  disease.  It  has  heen  suggested  that 
sexual  continence  in  high-strung  men  produces  changes  in 
tlie  nervous  system  which  can  conceivably  lead  to  the  pro- 
duction of  high  tension  and  further  to  arteriosclerosis.  This, 
however,  I  can  not  think  has  any  foundation  in  fact  except 
in  so  far  as  such  men  are  prone  to  live  at  high  speed  and 
wear  themselves  out  sooner  than  the  normal  jjerson.  The 
sexual  continence  i)e)-  se  is  not  harmful.  There  are,  how- 
ever, men  who  seem  not  to  l)e  harmed  by  the  constant  wear 
and  tear  of  our  modern  life.     These  are  the  exceptions. 

Workers  in  factories  where  paint  is  made  and  the  in- 


ETIOLOGY  1G3 

gredieiits  liaiKl-inixed,  are  prone  to  develop  arteriosclerosis 
early  in  life.  It  lias  been  found  that  the  laborers  most  apt 
to  be  victims  of  lead  intoxication  are  those  who  ai'e  careless 
in  their  habits  of  cleanliness,  particularly  in  reg'ard  to  the 
iingernails.  The  continuous  absorption  of  lead  into  the 
system,  brink's  about  a  condition  of  hyi^ei'tension  that  has 
its  inevita])le  results. 

The  fact  is  that  any  occupation  which  entails  either  the 
absorption  of  toxic  substances,  or  prolonged  muscular  la- 
bor, will  hasten  markedly  the  onset  of  arterial  disease. 

Food  Poisons 

The  opinion  that  arteriosclerosis  is  due  in  large  part  to 
poisoning  by  end  products  or  bj^-products  of  protein  di- 
gestion is  now  receiving  umcli  supj)ort.  Experiments  on 
dogs  and  ra])bits  have  lent  some  confirmation  to  chemical 
observations.  It  has  been  shown  that  dogs  fed  for  a  long 
time  on  putrefied  meat  developed  inflannnation  and  degen- 
eration of  the  adventitia  and  media,  with  hyperplasia  and 
calcification  of  the  intima  of  many  arteries.  In  the  pul- 
monary and  carotid  arteries,  in  the  vena  cavas  and  myo- 
cardium, there  were  extensive  necroses  and  hyaline  degen- 
eration. Moreover,  injections  of  sodium  urate  and  ergot 
caused  necroses  in  the  muscularis  and  elastica  of  the  aorta, 
pulmonary  artery,  vena  cavas  inferior  and  heart  muscle,  but 
there  was  no  calcification.  (luinea  pigs  which  were  fed 
indol  in  small  doses  by  the  mouth  over  a  long  period  showed 
atheromatous  degeneration  of  the  aorta. 

Infectious  Diseases 

As  more  study  has  been  given  to  the  arteries  in  persons 
who  have  died  of  the  acute  infectious  diseases,  more  has 
come  to  light  concerning  the  effects  of  the  toxins  of  these 
diseases  on  the  vessel  walls.  In  the  arteries  of  children 
who  have  died  of  measles,  scarlet  fever,  dii)htheria,  cere- 


164  ARTEPJOSCLEROSIS 

])rosi)iiial  meningitis,  etc.,  degenerative  changes  in  the  ar- 
teries occur,  modified  only  by  tlie  length  of  time  that  the 
toxins  have  acted. 

Thayer  has  shown  that  the  arteries  of  those  who  have 
passed  through  an  attack  of  moderately  severe  or  severe 
typhoid  fever  are  as  a  rule  more  readily  palpable  than  are 
the  vessels  of  persons  of  corresponding  years  who  have 
never  had  the  disease.  Clinically  the  typhoid  toxin  appears 
to  cause  the  early  production  of  arteriosclerosis,  Tlie 
changes  in  the  arteries  occur  for  the  most  part,  and  always 
earlier,  in  the  peripheral  arteries,  and  tlie  media  is  chiefly 
affected.  Minute  yellowish  patches  are  found  on  the  aorta, 
carotids,  and  coronaries.  In  persons  who  have  passed 
through  an  attack  of  one  of  the  fevers,  and  have  later  died 
from  some  other  cause,  regenerative  changes  are  sometimes 
found  to  have  taken  place  in  the  arteries,  consisting  of  an 
ingrowth  of  elastic  fibers  from  the  intact  adventitia  to  the 
diseased  media. 

That  there  are  some  other  factors  than  the  infectious  dis- 
ease which  are  concerned  in  the  production  of  arterial 
changes  seems  evident  from  a  study*  made  recently  among 
a  group  of  almshouse  inmates  ranging  in  age  from  38  to 
90  years.  The  study  included  500  persons  of  both  sexes. 
Careful  histories  were  taken  to  determine  the  presence  of 
antecedent  infectious  disease.  The  radial  artery  was  pal- 
pated to  deternune  the  presence  of  sclerosis.  Among  the 
cases  giving  a  history  of  one  infectious  disease  the  follow- 
ing table  gives  the  results : 


DISEASE 

NO. 

_i_ 

++ 

+++ 

POSITIVE 

NEGATIVE 

Measles 

■    47 

10 

(5 

12 

28 

19 

Infectious   artliritis        38 

9 

(5 

4 

19 

19 

Pneumonia 

30 

~) 

8 

5 

18 

12 

Typhoid 

27 

6 

8 

3 

17 

10 

Scarlet  fever 

10 

0 

0 

4 

4 

6 

Smallpox 

14 

1 

4 

0 

5 

9 

Miscellaneous 

12 

2 

5 

2 

9 

3 

178 

33 

37 

30 

100 

78 

^Warfield,    I<.    M. :    Jour.    Lali.    and    Clin.    Med.,    November,    1917. 


ETIOLOGY  1G5 

A  summary  of  the  cases  showed :  252  cases  without  sclero- 
sis; 248  with  sclerosis;  147  cases  with  infections  but  no 
sclerosis;  180  cases  with  infections  and  sclerosis. 

This  study  failed  to  throw  any  positive  light  on  the  ques- 
tion. Infectious  diseases  undoubtedly  play  a  certain  role, 
particularly  those  continuing  a  long  time  and  certain  par- 
ticular infectious  diseases,  as  measles. 

Syphilis 

Syphilis  is  one  of  the  most  important  of  the  etiologic 
factors  in  the  production  of  arteriosclerosis.  It  has  been 
shown  that  in  85  per  cent  of  cases  of  aortic  insufficiency  in 
persons,  usually  males,  over  forty-five  years,  who  did  not 
have  chronic  infective  endocarditis,  the  Wassermann  re- 
action was  positive.  Acute  aortitis  affecting  the  ascending 
and  transverse  portions  of  the  arch  of  the  aorta  is  very 
commonly  seen,  and  the  irregular,  scattered,  slightly  raised, 
yellowish-white  patches  of  sclerosis  in  the  arch  which  are 
found  years  after  the  syphilitic  lesion,  are  considered  by 
some  to  be  very  characteristic  of  syj)hilis.  Mesaortitis  is 
the  primary  lesion  and  acts  as  a  locus  minoris  resistentuc 
where  an  aneurysm  forms. 

Hypertensive  cardiovascular  cases  have  been  serologi- 
cally studied,  and  a  positive  Wassermann  reaction  found 
in  a  large  percentage  of  one  series.  In  fifty  cases,  90  per 
cent  either  gave  a  positive  Wassermann  reaction  or  luetin 
test,  were  known  to  have  syphilis,  or  had  children  with 
hereditary  syphilis.  This  suggests  what  might  be  called 
"familial  cardiovascular  syphilis." 

Hypertensive  disease  is  possibly  one  of  the  conmion  so- 
called  "late"  manifestations  of  syphilis.  That  syphilis  is 
responsible  for  the  arterial  disease  in  the  vessels  of  tlie 
brain,  resulting  in  apoplexy  or  sudden  cai'diac  death  in  mid- 
dle life,  has  long  been  known.  In  fact,  it  is  claimed  (Osier) 
that  all  aneurysms  occurring  in  persons  under  thirty  years 


166  APtTERIOSCLEROSIS 

of  age  are  due  to  syphilitic  aortitis.    In  the  late  stages  of 
sypliilis  tlie  arterial  lesions  may  he  of  a  diffuse  character. 

Chronic  Drug  Intoxications 

Lead,  tobacco,  and  according  to  some,  tea  and  coffee,  are 
to  l)e  classed  as  causal  factors  in  the  i^roduction  of  arterio- 
sclerosis. Certain  it  is  that  all  these  substances  have  a 
tendency  to  raise  the  arterial  pressure,  but  whether  the 
drug  itself  causes  first  a  degeneration,  and  later  a  hyperten- 
sion results,  or  vice  versa,  is  not  yet  positively  known. 
We  have  just  mentioned  that  lead  particularly  has  a  marked 
effect  in  producing  arterial  lesions.  Other  drugs  as  ad- 
renalin, l)ariuni  chloride,  pliysostigmin,  etc.,  while  produc- 
ing experimental  arteriosclerosis,  hardly  could  produce 
the  disease  in  man.  Alcohol  has  been  l)lamed  for  nuicli,  and 
as  an  etiologic  factor  in  the  production  of  arteriosclerosis 
formerly  was  accorded  a  first  place.  More  recently  much 
doubt  has  been  thrown  on  this  supposition  by  the  work  of 
Cabot,  who  showed  that  the  mere  drinking  of  even  large 
quantities  of  spirits  had  no  effect  in  producing  arterial 
disease. 

This  observation  has  been  recently  substantiated  by 
Hultgen,  who  carefully  studied  clinically  460  cases  of 
chronic  alcoholism.  He  says,  "There  are  no  cardiovascu- 
lar symptoms  which  might  be  termed  characteristic  of 
chronic  alcoholism,  unless  it  be  the  peculiar  fetal  qualities 
of  the  heart  sounds  which  we  know  as  embryocardia.  I 
find  this  very  frequent  among  drinkers,  ])ut  I  can  offer  only 
a  tentative  explanation  for  it,  namely  the  following:  Em- 
bryocardia can  only  occur  with  low  tension  blood  pres- 
sure, and  in  the  absence  of  renal  insufficiency.  Hence  it 
might  be  considered  as  a  useful  condition  of  no  pathologic 
significance  at  all.  That  alcohol  is  a  sclerogenic  iDliarmakon 
and  productive  of  arteriosclerosis  with  its  usual  train  of 
symptoms  may  be  a  fact,  but  its  demonstration  would  be 


ETIOLOGY  107 

difficult  and  is  really  not  sliowii  1)y  my  tabulations.  There 
were  cardiovascular  cliauft-es,  such  as  myocarditis,  aortitis, 
valvular  heart  disease  and  arteriosclerosis  in  chronic  alco- 
holics in  54.3  per  cent  of  461  cases,  but  this  by  no  means 
constitutes  a  proof  of  the  causal  relationship  between  these 
lesions  and  the  abuse  of  liquors.  I  believe  it,  nevertheless, 
to  be  good  reasoning-  to  ascril)e  the  bulk  of  cardiovascular 
symptoms  to  tlie  sclerogenic  action  of  alcohol,  while  ab- 
staining from  an  interi)retation  of  its  pathogenesis."  Just 
what  role  tobacco  inlays  is  difficult  to  say.  jMy  own  oj^inion 
is,  that  of  itself  when  used  in  moderation,  it  has  no  ill 
effects.  However,  as  tobacco  is  a  drug  that  may  raise  the 
blood  pressure,  excessive  use  nmst  be  held  responsible  for 
the  production  of  arteriosclerosis.  It  is  difficult  to  sepa- 
rate its  effects  from  those  produced  by  eating  and  drinking. 

Overeating 

There  can  be  no  doubt  but  that  the  constant  overloading 
of  the  stomach  with  rich  or  difficultly  digestible  food  is 
responsible  for  a  large  numlier  of  cases  of  arteriosclerosis. 
Every  one  must  have  noted  the  increase  in  foi'ce  and  volume 
of  the  heart  beat  after  the  ingestion  of  a  large  meal.  The 
constant  repetition  of  such  processes  conceivably  can  lead 
to  damage  to  the  vessel  walls  through  hypertension. 

In  the  metabolism  of  food  in  the  intestines  there  are  sub- 
stances produced  which  are  poisonous  when  absorbed  di- 
rectly into  the  circulation.  Ordinarily  these  substances 
are  rendered  harmless  either  before  absorption  or  are  de- 
toxicated  in  the  liver  to  harmless  substances.  It  is  con- 
ceivable that  a  constant  overproduction  of  such  poisons 
would  eventually  damage  the  defensive  mechanism  of  the 
body  to  such  an  extent  that  some  of  the  poisons  would 
circulate  in  the  blood.  An  expression  of  a  surplus  of  one, 
at  least,  of  these  decomposition  products  is  the  ap})earance 
of  indican  in  the  urine.  It  is  not  believed  that  indicanuria 
has  the  imiiortance  attached  to  it  which  some  authors  would 


]  68  ARTERIOSCLEROSIS 

have  ns  hcliovc.  It  is  found  too  often  and  in  too  many  vary- 
ing conditions,  nevertlieless  it  undoubtedly  does  reveal  tlie 
presence  of  perverted  metal)olism. 

In  liow  far  the  toxins  a])sorhed  from  the  intestinal  tract 
are  responsible  for  the  production  of  arterial  disease,  it  is 
not  possible  to  say.  Some  observers  lay  great  stress  on 
this  factor  as  a  cause  of  arteriosclerosis.  The  author  be- 
lieves that  tlie  role  played  by  the  absorption  of  products  of 
perverted  intestinal  metabolism  is  an  important  one.  The 
primary  change  is  an  increased  tension  in  the  arterioles 
which  later  leads  to  thickening  of  the  coats  of  the  vessels 
and  to  the  other  consequences  of  arterial  disease.  A  vi- 
cious circle  is  thus  established  which  has  a  tendency  to  be- 
come progressively  worse. 

Mental  Strain 

More  and  more  does  one  become  impressed  with  the  fact 
that  patients  with  arteriosclerosis  are  very  often  those  who 
take  life  too  seriously  and  either  from  ambition  or  from  an 
exalted  sense  of  duty  lead  especially  strenuous  lives.  Not 
always  are  these  persons  addicted  to  drug  or  liquor  habit. 
Many  are  rather  abstemious  in  their  habits.  It  is  not  so 
often  that  we  see  as  a  victim  of  arteriosclerosis,  the  care- 
free person  who  laughs  liis  way  through  life  without  worry- 
ing about  the  morrow.  He  is  not  so  prone  to  arteriosclero- 
sis. Worry  is  a  far  more  potent  cause  of  breakdown  than 
actual  manual  work.  It  is  tlie  rule  to  find  thickened  arteries 
among  neurasthenics.  This  may  l)e  only  part  of  a  general- 
ized degeneration  of  all  tissue  in  the  body.  The  blood  pres- 
sure in  such  persons  is  usually  low.  So  many  men  of  our 
better  class  live  under  a  continuous  mental  strain  in  the 
business  world.  The  increase  in  arteriosclerosis  cases  is 
real,  not  apparent.  The  intense  mental  strain  seems  to  cause 
a  marked  increase  in  blood  jjressure  (for  short  periods  of 
mental  effort  this  has  been  proved)  over  a  period  of  time 


ETIOLOGY  169 

sufficient  to  cause  permanent  changes  in  the  vessel  walls. 
The  same  sequence  of  events  repeats  itself;  hioh  tension, 
arterial  strain,  compensatory  thickening,  hypertrophiod 
heart,  etc. 

Certainly  the  character  of  the  arterial  tissue  has  much  to 
do  witli  the  determination  of  degenerative  changes  Avhich 
may  result  from  the  action  of  one  or  more  of  the  etiologic 
factors. 

Muscular  Overwork 

Muscular  overwork  is  to  he  reckoned  with  as  an  etiologic 
factor.  One  sees  it  especially  among  the  laboring  class  in 
both  whites  and  negroes.  Possibly  other  factors,  as  alco- 
hol and  coarse  heavy  food,  contribute  to  the  early  arterial 
degeneration.  Hypertrophy  of  the  heart  occurs  in  athletes, 
and  statistics  gathered  among  the  oarsmen  especially,  show 
a  relatively  liigh  mortality  at  the  different  decades  trace- 
able to  the  high  tension  produced  while  in  training.  This 
question  deserves  more  consideration  than  has  been  ac- 
corded it. 

Renal  Disease 

Chronic  disease  of  the  kidneys  (contracted  red  kidney)  is 
one  of  the  most  certain  producers  of  hypertension;  in  fact, 
some  maintain  that  high  tension,  even  without  demonstra- 
ble kidney  lesions,  as  revealed  by  careful  urine  examina- 
tions, is  a  valuable  sign  pointing  to  chronic  nephritis.  This 
is  doubted  by  others,  myself  among  them.  Just  what  causes 
tlie  increase  in  blood  pressure  sometimes  to  over  270  mm. 
of  Hg,  is  not  definitely  known.  It  seems  most  probable  that 
it  is  some  poison  elaborated  ])y  the  diseased  kidneys  and 
absorbed  into  the  general  circulation.  There  it  acts  pri- 
marily on  the  musculature  of  the  arterioles  causing  tonic 
contraction  and  an  increase  of  work  on  the  part  of  the  lieart 
to  force  the  blood  through  narrowed  channels.  One  fact  is 
certain.    We  see  patients  in  coma  due  to  renal  disease  with 


170  APiTERIOSCLEROSIS 

blood  pressure  iiiueli  over  200  iiiiii.  of  Kg.  As  these  cases 
clear  up,  the  pressure  uiay  fall,  and  should  they  seemingiy 
recover,  the  recovery  is  accompanied  witli  a  marked  de- 
crease in  blood  pressure,  finally  reaching-  the  normal  for 
the  individual.  IMoreover,  in  tlie  course  of  a  severe  acute  or 
sub-acute  nephritis,  hypertension  is  associated  with  head- 
ache, partial  or  total  blindness,  and  drowsiness.  AVhen  the 
pressure  is  reduced,  all  these  symptoms  disappear. 

There  is  also  the  chronically  shrunken  and  scarred  kid- 
ney known  jjathologically  as  the  arteriosclerotic  kidney. 
It  is  j^robable  that  there  are  two  groups  of  cases  which  we 
may  designate:  (1)  j^rimary;  (2)  secondary.  In  the  pri- 
mary group  the  kidney  disease  antedates  the  sclerosis  of 
the  arteries,  and  the  sclerosis  is  most  probably  dependent  on 
the  constant  high  tension.  AV(^  know  that  prolonged  hyper- 
tension will  produce  severe  forms  of  arteriosclerosis.  The 
arterial  disease  in  this  group  is  caused  by  the  renal  disease. 

In  the  second  group  the  kidney  changes  are  apparently 
due  to  the  general  ai'teriosclerosis  which,  affecting  the  kid- 
ney vessels,  causes  changes  leading  to  atrophy  and  subse- 
quent fibrous  tissue  ingrowth  of  scattered  areas.  These 
cases  are  not  necessarily  associated  with  hypertension;  on 
the  contrary  there  is  more  apt  to  be  hypotension.  AVliere 
the  first  group  occurs  for  the  most  part  in  young  and  active 
middle-aged  people,  the  second  group  is  the  result  of  in- 
volutionary  processes  which  accompany  advanced  age. 

However  careful  a  urinalysis  may  be,  there  is  no  assur- 
ance that  one  can  predict  the  pathologic  state  of  the  kidney. 
Often  so-called  normal  urine  will  be  secreted  by  a  badly 
diseased  kidney,  whereas  a  urine  which  contains  considera- 
l)le  albumin  and  many  casts  may  be  secreted  by  a  kidney 
which  is  only  temporarily  the  seat  of  infiannnation.  AVliat 
matters  after  all  is  not  the  state  of  the  kidney  which  the 
pathologist  desc]-il)es,  but  the  actual  functional  response 
of  the  kidney  in  the  body  to  the  various  tests  now  w^ell 
known. 


ETIOLOGY  171 

Ductless  Glands 

At  tlie  2»'e«eiit  time  the  tendency  among  some  writers 
is  to  make  the  ductless  glands  tlie  resj^onsible  agents  in 
almost  all  diseases.  Arteriosclerosis  is  no  exception  to  this 
tendency.  Sajous,  for  example,  divides  the  morbid  process 
producing  arteriosclerosis  into  three  types;  (1)  autolytic, 
(2)  adrenal,  (3)  denutrition.  In  the  first  type  he  finds 
the  pancreas  to  be  the  most  important  gland.  It  supplies 
an  internal  secretion  which  ''takes  a  direct  part  in  the  pro- 
tein metabolism  of  the  tissue  cells,  and  also  in  the  defensive 
reactions  within  tliese  cells,  as  well  as  in  the  phagocytes  and 
in  the  blood  stream."  This  being  the  case  exaggeration  of 
this  digestive  process  has  tissue  destruction  as  its  result, 
arteriosclerosis  among  them. 

In  the  adrenal  type  Sajous  argues  that  adrenalin  pro- 
duces lesions  experimentally,  therefore  the  adrenal  gland 
has  a  profound  influence  by  its  internal  secretion  in  connec- 
tion with  the  sympathetic  system  in  producing  degenera- 
tions leading  to  arteriosclerosis. 

The  denutrition  type  has  as  its  particular  gland  the  thy- 
roid. The  sclerotic  process  in  the  arteries  is  due  to  the  lack 
of  thyroid  as  in  cases  of  myxedema.  After  a  long  resume 
of  his  ideas  he  concludes  "that  arteriosclerosis  is  the  result 
of  excessive  or  deficient  activity  of  certain  ductless  glands, 
the  thyroid  and  adrenal  in  particular." 

No  one  can  dogmatically  deny  the  part  which  the  ductless 
glands  may  play  in  the  production  of  arteriosclerosis,  but  it 
hardly  seems  that  there  is  enough  actual  experimental  evi- 
dence to  show  that  they  take  such  an  important  pai't  as  Sa- 
jous  l)elieves.  Until  further  and  more  convincing  evidence 
is  offered  l)y  competent  investigators,  I  prefer  to  look  with 
some  skepticism  upon  the  ductless  gland  theory  of  the  caus- 
ation of  arteriosclerosis.  The  field  lends  itself  too  easily 
to  speculation  and  imagery.  Some  are  already  allowing 
themselves  the  mental  debauch  of  this  nature. 


CHAPTER  VII 

THE  PHYSICAL  EXAMINATION  OF  THE  HEART 
AND  ARTERIES 

Heart  Boundaries 

111  order  to  be  able  to  estimate  the  departures  from  nor- 
mal in  the  boundaries  of  the  heart,  it  is  essential  that  there 
be  a  definite  appreciation  of  the  boundaries  of  the  normal 
heart  in  relation  to  the  chest  wall. 

It  is  frequently  stated  that  the  right  limit  of  cardiac  dull- 
ness is  normally,  in  the  adult,  just  at  the  right  border  of 
the  sternum.  This  is  not  strictly  accurate.  Careful  dis- 
sections at  the  autopsy  table  and  x-ray  plates  of  the  chest 
made  at  a  distance  of  two  meters  from  the  tube  show  that 
the  border  of  the  right  auricle  is  from  one  to  one  and  a 
half  and  even  two  centimeters  from  the  edge  of  the  sternum 
at  the  level  of  the  fourth  rib,  and  on  the  living  subject  this 
can  be  also  demonstrated.  The  right  border  of  the  heart 
usually  is  from  3  to  4  cm.  from  the  midsternal  line  at  the 
level  of  the  fourth  rib. 

Again  there  is  a  term  used  in  defining  the  apex,  known  as 
the  point  of  maximum  impulse.  As  this  does  not  always 
coincide  with  the  apex  beat  and  with  the  outer  lower  left 
border  of  the  heart,  it  would  be  better  to  use  the  term  apex 
beat. 

Normally,  then,  the  cardiac  dullness,  the  so-called  relative 
cardiac  dullness,  begins  above  at  the  upper  border  of  the 
third  costal  cartihige,  as  a  rule,  and  taking  a  somewhat 
curved  line  with  the  concavity  inward,  descends  to  the  fifth 
interspace  or  beneath  the  fifth  rib  from  9  to  10  cm.  from  a 
line  drawn  through  the  center  of  the  sternum  parallel  to  its 
length,  the  midsternal  line.  This  seems  to  me  to  be  a  bet- 
ter method  of  recording  the  size  of  the  heart  than  by  the 

172 


PHYSICAL   EXAMTXATIOlSr    OF    HEART    AXD   ARTERIES         173 

lines  commonly  used;  viz.,  the  nipple,  or  midclavicular,  or 
parasternal  line.  Below,  the  cardiac  dullness  is  merged  into 
the  tympany  from  the  stomach  and  the  dullness  from  the 
liver.  At  the  sixth  right  costosternal  articulation  there  is 
a  sharp  turn  upwards  forming  at  that  point  with  the  liver 
the  cardiohepatic  angle.  At  the  fourth  right  cartilage  or 
the  third  interspace,  the  dullness  is  from  one  to  two  centi- 
meters from  the  edge  of  the  sternum.  We  have  then  a  some- 
what pear-shaped  area  or  triangular  area  with  the  apex  at 
the  apex  of  the  heart.  The  so-called  absolute  cardiac  dull- 
ness does  not  appear  to  me  to  be  of  any  great  significance. 
In  reality  it  is  the  limit  of  lung  resonance  and  may  be 
greater  or  less,  not  so  much  on  account  of  variations  in  the 
size  of  the  heart,  as  of  variations  in  size  of  the  lungs  and 
shape  of  the  chest  wall. 

The  really  crucial  question  which  should  always  be  asked 
is.  Is  the  heart  enlarged  or  decreased  in  size  ?  The  position 
of  the  apex  beat  alone  can  not  determine  this,  neither  can  the 
limit  to  the  right  of  the  stern  am.  The  distance  between 
these  two  points  and  the  depth  of  the  dullness  at  a  distance 
of  5  cm.  from  the  midsternal  line  on  the  left  side,  will  give 
the  size  of  the  heart  as  nearly  as  can  be  obtained  in  the  liv- 
ing subject.  A  series  of  measurements  in  normal  adults 
average  13  to  14  cm.  and  9  to  10  cm.  respectively.  For 
women  they  are  about  1  cm.  less  in  each  direction. 

The  elaborate  mechanism  known  as  the  orthodiagraph  is 
probably  the  best  means  of  determining  the  actual  limits 
of  the  heart,  but  few  men  have  such  an  expensive  instru- 
ment, and,  moreover,  at  the  bedside  such  an  instrument 
could  not  be  used.  From  comparative  measurements  I  con- 
cur in  the  belief  of  those  who  affirm  that  careful  percussion 
will  furnish  equally  as  accurate  limits. 

The  first  step  in  making  an  examination  of  the  heart  is  to 
expose  the  patient's  chest  in  a  good  light,  and,  sitting  at  his 
right  side,  carefully  inspect  the  chest.  The  position  of  the 
apex  beat,  heaving,  bulging,  retraction  of  interspaces,  etc., 


1 74  AirrFJtiosci.Eiiosis 

can  easily  1h'  seen  ii'  visil)le.  After  careful  inspection  has 
i>'iven  all  the  data  wliicli  it  is  ])()ssil)le  to  ohtain,  one  next 
lays  the  i)alni  of  the  hand  over  the  lieai't  and  attempts  to 
])al])ate  the  a]»ex  l)eat.  The  thrust  of  the  a])ex  in  a  liyper- 
tro])hied  heart  can  readily  be  felt,  and  one  can  feel  whether 
the  heart  is  regular,  irregular,  intermittent,  or  has  other 
change  in  rhythm.  The  shock  of  the  closing  valves,  particu- 
larly the  aortic,  can  he  felt,  and  that  and  the  foi'cil)le  apical 
impulse  are  very  suggestive  signs  of  hypertrophy  and 
liy]iei*tension.  Thrills  may  also  he  felt  and  can  he  timed 
in  relation  to  the  heart  cycle. 

Percussion 

It  is  to  percussion  that  we  next  proceed,  and  for  the  data 
in  regard  to  the  size  of  the  heart,  it  is,  for  our  purpose,  the 
most  valual)le  of  all  the  i)liysical  methods  of  heart  examina- 
tion. 

First  and  foremost  we  wish  by  percussion  to  learn  the 
actual  size  of  the  heart,  in  other  words  what  is  ordinarily 
called  the  relative  cardiac  dullness.  With  the  absolute  dull- 
ness we  are  not  concerned.  That  irregular  area  represents, 
as  has  been  said,  actually  the  limits  of  lung  resonance.  The 
heart  may  or  may  not  be  covered  w^itli  lung;  there  may  or 
may  not  be  the  incisura  cardiaca.  What  I  wish  to  insist 
upon  is  that  the  size  of  the  area  of  absolute  dullness  can 
give  us  no  data  in  regard  to  the  size  of  the  heart.  What  we 
must  endeavor  to  learn  is  the  actual  size  of  the  heart  as 
nearly  as  our  crude  means  will  permit. 

Light,  very  light,  almost  inaudible  percussion,  what  Gold- 
scheider  called  "  Schwellungsperkussion, "  must  be  prac- 
ticed. Use  the  middle  finger  of  the  right  (left)  hand  as  the 
hammer  and  the  last  joint  of  the  middle  finger  of  the  left 
(right)  hand  pressed  firmly  against  the  cliest,  as  pleximeter. 
I  believe  it  is  better  to  place  the  pleximeter  finger  parallel 
to  the  boundary  to  be  limited  although  some  place  the  finger 
perpendicularly,   that  is,  pointing  toward   the  boundary. 


riTYSICAL    EXA^nXATIOX    OF    ITEAPiT    AND    ATtTERlKS         175 

Now  and  tlioii  it  helps  to  l)on(l  tlie  iiloxiniotci-  rni<i,(M-  at  tlio 
second  joint,  liold  it  i^erpendiciilarly  to  tlio  clicst  wall,  and 
strike  the  joint  directly  in  line  of  the  finger.  This  in  my 
hands  has  ])een  of  great  assistance  in  percnssing  the  limits 
of  the  heart  dullness.  Pottenger's  "light  touch  palpation" 
is  a  modification  of  the  light  palpation  and,  to  my  mind,  has 
no  very  sj^ecial  advantages.  Auscultatory  i^ercussion  is  of 
great  value  at  times.  The  ])ell  of  the  stethoscope  is  placed 
over  the  portion  of  heart  uncovered  hy  lung  (should  sucli 
l)e  the  case),  and  with  this  point  as  a  center  the  chest  is 
lightly  and  quickly  tapj^ed  along  radii  converging  toward 
the  stethoscope.  One  soon  learns  to  recognize  the  change 
of  pitcli  as  the  tapping  reaches  tlie  border  of  the  lieart.  It 
is  well  to  use  all  methods,  especially  in  difficult  cases,  and 
to  comj^are  the  results.  Personally  I  have  found  that  hy 
light  percussion  I  can  limit  with  nmch  accuracy  the  upper, 
riglit,  and  left  borders  of  the  heart. 

There  is  nuich  to  be  gained  l)y  using  light  i^ercussion. 
Strong  blows  set  in  vi])ration  not  only  the  underlying  struc- 
tures, but  also  more  or  less  of  the  chest  wall.  AVe  wish  to 
avoid  this  source  of  error,  we  do  not  wish  to  differentiate  by 
pitch  alone.  Finally  one's  pleximeter  finger  becomes,  after 
long  practice,  so  sensitive  to  changes  in  the  resonance  of 
structures  lying  below  it,  that  there  is  actual  feeling  of  im- 
pairment to  the  slightest  degree.  This  delicate  touch  is 
what  we  should  endeavor  to  cultivate. 

It  is  at  times  of  advantage  to  use  immediate  percussion. 
This  is  done  by  bending  the  fingers  of  the  striking  hand, 
bringing  the  tips  in  a  line  and  striking  the  chest  lightly  with 
the  four  fingers  as  one  finger.  Some  find  it  easier  to  per- 
cuss the  dullness  due  to  the  heart  in  this  way  than  by  medi- 
ate percussion. 

The  little  hammer  and  hard  rubber,  celluloid,  bone,  or 
ivory  pleximeter  does  not  seem  to  me  to  be  nearly  as  good 
as  the  fingers.  Moreover,  one  always  has  his  hands,  but 
may  forget  his  hannner  and  ijleximeter. 


176  ARTERIOSCLEROSIS 


Auscultation 


In  auscultating  tlie  heart  I  prefer  the  binaural  stetho- 
scope of  the  Ford  pattern.  The  recent  substitution  of  an 
aluniinum  bell  for  tlie  hard  rubber  bell  is  an  improvement. 
Personally  I  do  not  favor  the  phonendoscope  or  any  of  the 
new  patent  non-roaring  instruments  now  for  sale  by  urgent 
instrument  makers.  The  phonendoscope  has  its  uses,  for 
example  in  auscultating  the  back  when  a  patient  is  lying 
in  bed  or  in  listening  to  the  heart  sounds  when  a  patient  is 
under  an  anesthetic;  but  for  differentiating  tlie  murmurs 
and  for  heart  diagnosis,  I  much  prefer  the  regular  bell 
stethoscope. 

In  arteriosclerosis  the  two  places  over  which  it  is  impor- 
tant to  listen  are  the  apex  and  the  second  right  cartilage, 
the  aortic  area.  Over  the  former,  one  gains  data  in  regard 
to  the  strength  of  the  heart  as  indicated  by  the  first  sound, 
over  the  latter  point,  one  learns  of  the  tension  in  the  aorta 
by  the  character  of  the  sound  produced  when  the  aortic 
valves  close. 

The  hypertrophy  of  the  heart  in  arteriosclerosis  is  in- 
variably due  to  the  enlargement  and  thickening  of  the  left 
ventricle.  From  the  nature  of  the  position  which  the  heart 
assumes  in  the  thorax,  this  enlargement  is  downward  and 
to  the  left.  The  apex  beat  will  therefore  be  found  in  the 
fifth  or  sixth  interspace,  and  definitely  at  an  increased  dis- 
tance from  the  midsternal  line.  As  stated  above,  it  is 
most  important  that  this  distance  be  accurately  measured 
and  put  down  in  the  notes  of  the  case  for  future  reference. 
No  satisfactory  prognosis  can  be  given  unless  this  is  done, 
for  the  gradual  increase  or  the  decrease  under  treatment  in 
the  size  of  the  heart  can  thus  be  definitely  known,  and, 
knowing  tlie  other  factors,  a  prognosis  may  be  given  which 
will  be  of  some  value  to  the  patient. 


PHYSICAL   EXAMINATION    OF    HEART    AND    ARTERIES         177 

The  Examination  of  the  Arteries 

It  is  exceedingly  difficult  at  times  to  affirm  definitely  that 
an  artery,  the  radial  for  examjole,  is  actually  sclerosed. 
Much  depends  on  the  sensitiveness  of  the  fingers  of  him 
who  palpates,  and  much  upon  the  relation  of  the  palpated 
artery  to  the  surrounding,  chiefly  underlying,  structures. 
In  the  examination  of  arteries  it  is  well  to  inspect  the  body 
for  the  pulsations  caused  by  them.  Frequently  an  exceed- 
ingly tortuous  artery,  such  as  the  brachial,  may  be  seen 
throughout  its  whole  extent  and  yet  the  radial  appear  lit- 
tle, if  any,  thickened  by  paljjation.  Again  the  artery  of  a 
pulse  of  high  tension  which  is  small  in  size  but  full  between 
the  beats,  may  not  be  as  sclerosed  as  one  wdiich  collapses 
and  feels  much  softer.  It  is  difficult  to  obtain  accurate  data 
in  regard  to  the  tension  in  an  artery  by  feeling  it  with  the 
fingers  of  one  hand.  One  should  use  both  hands.  With  the 
middle  finger  of  the  right  (left)  hand  the  artery  is  com- 
pressed peripherally,  that  is,  nearest  the  wrist.  The  blood 
is  then  pressed  out  of  the  artery  with  the  middle  finger  of 
the  left  (right)  hand,  so  as  to  obliterate  completely  the 
pulse  wave  and  the  two  or  three  inches  between  the  middle 
fingers  are  felt  with  the  index  fingers.  By  holding  the  fin- 
ger firmly  on  the  artery  near  the  wrist  so  as  to  block  any 
wave  that  may  come  through  the  palmar  arch  by  anastomo- 
sis with  the  ulnar  artery  and  by  releasing  pressure  on  the 
proximal  middle  finger,  some  idea  may  be  had  of  the  degree 
of  pulse  tension.  However,  no  amount  of  practice  can  more 
than  approximate  the  tension  and  when  one  is  surest  that 
he  can  tell  how  many  millimeters  of  pressure  there  are,  he 
is  apt  to  be  farthest  wrong  when  he  checks  his  guess  with 
the  sphygmomanometer. 

Much  may  be  learned  from  carefully  palpating  the  periph- 
eral arteries,  and,  as  a  rule,  the  sclerosis  of  these  arteries 
means  genera]  arteriosclerosis,  although  there  are  many 
exceptions  to  this. 


178 


Ar.TErtlOSCLEKOSIS 


A  more  recent  inclliod,  and  one  wliicli  in  llio  autltor's 
liaiuls  lias  IxM'ii  Found  to  Ix'  valual)le,  is  tliat  j)roposed  ])y 
Worllieiin-SaloJiionson  wlio  palpates  tlie  artery  not  witli 
the  ball  of  tlie  lin<;-er  l)ut  Avitli  tlie  iin<;-ernail.    The  fiiift-er  is 


I''ig.    57. — A   method   of   ringcr-tip   ]iaI|)ation   of  the   radial   artery.      (dravcs.) 


I'iiif.   5S. — AiiotluT  iiKtliiid   of   linRcr-ti])   palpation   of  the   radial   artery.      (Graves.) 

held  so  that  tlie  nail  is  perpendicular  to  the  surface  of  the 
skin  and  the  artery  is  felt  with  the  end  of  the  nail.  The  sen- 
sation is  j)erceived  at  the  root  and  makes  use  of  all  the  sensi- 
tive nerve  endings  there.    In  this  way  it  is  possible  to  feel 


PHYSICAL    EXAMINATIOX    OF    TTEAr.T    AND    ARTERIES         179 

tlie  arterial  wall  tlistiiictly,  and  a  little  practice  will  enable 
one  to  determine  wlietlier  or  not  the  vessel  Avail  is  thickened. 
It  is  also  possible  to  determine  Avitli  a  considerable  degree  of 
accuracy  the  diameter  of  the  artery  and  the  size  of  the  wall 
when  the  current  is  cut  off  by  pressure  on  the  j^roximal  side 
of  the  artery.  It  is  ])est  to  have  a  firm  background  when 
this  "fingernail"  palpation  is  used.  This  may  be  obtained 
by  i3alpating  the  radial  artery  against  the  loAver  end  of  the 
radius. 

Probably  the  best  method  of  palpating  the  arteries,  es- 
pecially the  radial,  to  determine  the  degree  of  sclerosis  and 
thickening,  is  to  use  the  tip  of  the  finger  and  roll  it  care- 
fully over  the  artery.  The  tip  of  the  finger  is  exceedingly 
sensitive  and,  moreover,  it  is  a  firmer  palpating  surface 
than  the  ball,  thus  enabling  one  to  appreciate  degrees  of 
sclerosis  which  could  not  ])e  differentiated  by  palpation 
with  the  soft  yielding  l)all.  This  finger  tip  palpation  is  well 
illustrated  in  the  figures  here  shown.     (Figs.  57  and  58.) 

Estimation  of  Blood  Pressure 

It  nmst  be  borne  in  mind  at  the  outset  that  arteriosclero- 
sis and  high  blood  pressure  are  not  always  associated.  As 
a  matter  of  fact  in  the  severest  grades  of  senile  arterio- 
sclerosis the  l)lood  pri^ssure  is  usually  below  the  normal 
for  the  individual's  years.  However,  as  liigh  tension  is  a 
frequent  factor  in  the  production  of  arterial  thickening, 
1)1  ood  pressure  readings  are  of  imjjortance. 

The  instrument  which  one  uses  is  of  minor  importance 
provided  it  is  proj^erly  standardized.  The  most  important 
feature  of  the  instrument  is  the  cuff.  This  must  be  12  cm. 
wide  and  be  long  enough  to  wraj^  around  the  arm  several 
times  so  that  the  j^ressure  is  evenly  distributed  over  the 
whole  arm  and  not  over  a  small  portion.  One  mercury  in- 
strument we  had  in  the  hospital  was  reported  to  ])e  at  great 
variance  with  a  dial  instrument.  This  mercury  instrument 
was  jirovided  with  a  cuff  which  was  short  and  was  tied 


180  AETEPJOSCLEROSIS 

around  tlio  arm  by  ineans  of  a  piece  of  tape.  Tliis  caused 
a  tifi'lit  constriction  over  a  small  area  and  rendered  the  es- 
timation too  liigli.  A  new,  long  tailed  cuff  easily  remedied 
tlie  a])parent  defect  in  the  instrument. 

In  taking  blood  pressures  the  difference  from  day  to  day 
of  10  or  even  15  mm.  of  systolic  pressure  has  no  great  sig- 
nificance. Fluctuations  of  the  systolic  pressure  alone,  it  is 
insisted  upon,  have  very  little  meaning.  One  must  take  the 
whole  pressure  picture  into  consideration  and  determine 
how  the  picture  changes  in  order  to  draw  any  conclusion  in 
regard  to  the  state  of  the  blood  pressure.  Failure  to  pay 
attention  to  this  evident  point  has  caused  much  futile  work 
to  be  written  and  published. 

It  is  well  to  emphasize  again  the  point  that  tlie  blood 
pressure  picture  consists  of  the  systolic,  the  diastolic,  the 
pulse  pressure  and  the  pulse  rate. 

Palpation 

Hoover  has  called  attention  to  the  direct  palpation  of  the 
femoral  artery  just  below  Poupart  's  ligament  as  a  more  ac- 
curate index  of  the  pressure  in  the  aorta  than  the  palpation 
of  the  radial  artery.  Possibly  one  can  obtain  a  more  ac- 
curate estimate  of  the  blood  pressure  in  this  way.  This, 
however,  is  open  to  dispute.  To  estimate  the  blood  pres- 
sure by  palpating  the  radial  artery  is  most  deceptive.  In 
about  75  per  cent  of  cases  one  can  tell  fairly  well  whether 
the  pressure  is  abnormally  high  or  abnormally  low.  Small 
variations  are  impossible  to  determine.  Unquestionably  it 
is  most  advantageous  to  get  into  the  habit  of  palpating  the 
femoral  artery  and  checking  the  result  with  the  sphyg- 
momanometer so  that  the  fingers  may  be  trained  to  appre- 
ciate as  accurately  as  possible  changes  of  pressure. 

It  may  be  that  one  day  when  the  instrument  is  needed  it 
is  not  at  hand.  A  well-trained  touch  then  becomes  a  great 
asset. 


PHYSICAL   EXAMINATIOjST    OF    HEART    AND    ARTEmES         181 

Precautions  When  Estimating  Blood  Pressure 

There  are  certain  precautions  which  must  be  strictly  ob- 
served when  deductions  are  drawn  from  tlie  manometer 
readings.  Tlie  jisycliic  factor  nuist  be  reckoned  with.  Any 
emotion  may  cause  marked  variations  in  the  pressure.  Ex- 
citement and  anger  are  especial  sources  of  error.  Even  the 
slight  excitement  arising  from  taking  the  first  blood  pres- 
sure on  a  nervous  patient  especially  is  apt  to  give  false 
values.  Usually  the  readings  must  be  taken  many  times  at 
the  first  sitting  and  the  first  few  may  have  to  be  set  aside. 
Worry  is  a  potent  factor  in  raising  the  pressure.  A  walk 
to  the  physician's  office,  especially  if  rapid,  has  its  effect. 

The  position  of  the  joatient  when  tlie  blood  pressure  is 
taken  is  important.  Usually  in  the  office  the  ijressure  is 
taken  when  the  patient  sits  in  a  chair.  He  should  assume  a 
relaxed,  comfortable  attitude.  The  readings  should  be 
made  at  the  same  time  of  day  and  at  the  same  interval  be- 
tween meals.  The  jjressure  in  both  arms  should  be 
measured  and  comparisons  should  be  made  only  between 
readings  on  the  same  arm.  These  precautions  may  seem 
useless  and  even  somewhat  trivial,  and  the  conditions  dif- 
ficult to  control.  But  unless  they  are  carefully  observed  the 
readings  will  be  false,  no  comparisons  can  l)e  drawn  l)e- 
tween  tlie  readings  on  different  daja,  and  the  instrument 
will  most  probably  be  blamed.  I  have  known  this  to  hap- 
pen so  often  that  I  can  not  emi^hasize  too  strongly  the  im- 
portance of  controlling  all  the  essential  conditions  which 
go  to  make  accurate  work. 

The  Value  of  Blood  Pressure 

In  the  past  few  years  there  has  been  a  veritable  ava- 
lanche of  blood  pressure  instrument  salesmen  who  have 
covered  the  country,  sold  instruments,  and  have  made  many 
startling  claims  for  the  instrument.  They  have  emj^hasized 
its  value  out  of  proportion  to  what  the  instrument  can  do 


182  ARTERIOSCLEROSIS 

even  in  the  liands  of  one  familiar  witli  all  the  defects.  Con- 
sequently it  is  not  necessary  to  emphasize  the  value  of  l)lood 
pressure.  It  seems  Ijest  to  utter  a  few  words  of  caution  in 
regard  to  its  interpretation. 

The  value  lies  not  in  the  occasional  estimation  compared 
with  some  other  one  reading,  but  in  the  frequent  estimation 
and  in  the  visualization  of  the  Idood  pressure  picture.  For 
the  great  majority  of  diseases  the  blood  pressure  has  no 
particular  value  except  to  show  that  the  circulation  is  not 
materially  disturbed.  The  limits  of  normal  are  rather  wide, 
so  that  consideration  of  the  jjatient's  age,  sex,  build,  etc., 
will  give  us  some  idea  of  a  base  line,  so  to  speak,  for  any  one 
person,  AVide  departures  from  relatively  normal  figures 
are  important,  but  are  not  diagnostic  or,  rather,  pathogno- 
monic. I  can  not  help  but  feel  that  the  diastolic  pressure  is 
the  most  important  part  of  the  blood  pressure  picture.  Per- 
sistent high  diastolic  pressure  means  increased  work  for  the 
heart,  which,  if  acting  for  a  long  time  against  the  high 
peripheral  resistance,  must  eventually  hypertrophy.  The 
arteries  become  thickened,  lose  their  wonderful  elasticity, 
fibrous  tissue  is  deposited  in  their  walls,  and  the  vicious 
circle  is  established  which  leads  to  pathologic  hypertension. 

Blood  pressure  readings  must  be  intimately  mixed  with 
brains  in  order  to  be  of  any  great  value  in  diagnosis  or 
prognosis. 


CHAPTER  A^ITI 
SYMPTOMS  AXU  PHYSICAL  SIGNS 

General 

AVell  developed  arteriot^elerosis  shows  four  patlioii^-no- 
iiionic  si,i>iis:  (1)  liypcrtropliy  of  the  heart;  (2)  aceentua- 
tion  of  tlie  aortic  second  sound;  (3)  palpa))k'  tliickenin<;-  of 
the  arteries;  and  (4)  hei,<^'litened  l)h)od  pressure.  However, 
it  nmst  not  be  inferred  that  tliese  sii^ns  nuist  ])e  present  in 
order  to  diagnose  arteriosclerosis.  It  has  already  been  said 
that  a  very  marked  degree  of  thickening,  with  even  calcifi- 
cation of  the  palpal)Ie  arteries,  may  occur  with  al)solutely 
no  increase  of  l)lood  pressure,  au'd  at  autopsy  a  small  flabby 
heart  may  be  found. 

While  arteriosclerosis  is  usually  a  disease  which  is  of 
slow  maturation,  nevei-theless  cases  are  occasionally  seen 
which  develo])  rather  ra])idly.  The  ])eripheral  arteries  have 
been  noticed  to  become  stiff  and  hard  in  as  relatively  biief 
a  time  as  two  yeai-s  from  the  recognized  onset  of  the  disease. 

Since  involution  processes  are  ])liysiologic,  as  has  been 
described  (vide  infra),  arteriosclerosis  may  assume  an 
advanced  grade  and  run  its  course  devoid  of  symptoms 
referable  to  diseased  arteries.  It  is  doubtful  whether  the 
sclerosis  itself  could  produce  symptoms,  exce])t  in  cases 
later  to  be  described,  were  it  not  that  the  organs  sui)plied 
by  the  diseased  arteries  suffer  from  an  insufficient  blood 
supply  and  the  symptoms  then  become  a  i)art  of  the  symp- 
tom-complex of  any  or  all  the  affected  organs. 

There  are  cases,  however,  in  comparatively  young  ])er- 
sons  where  a  combination  of  certain  ill-defined  svin])lonis 
gives  a  clue  to  the  underlying  i)atIiologic  i)rocesses.  These 
symptoms  of  early  arteriosclerosis  are  the  result  of  slight 

183 


184  ARTERIOSCLEROSIS 

and  variable  disturbances  in  tlie  circulation  of  the  various 
organs.  Xoi-mally  there  are  frequent  changes  in  the  blood 
pressure  in  the  organs,  but  the  vasomotor  control  of  normal 
elastic  vessels  is  so  perfect  that  no  symptoms  are  noted  by 
tlie  individual.  AVhen  the  arteries  are  sclerosed,  they  are 
less  elastic  and  the  blood  supply  is,  therefore,  less  easily 
regulated.  At  times  symptoms  occur  only  after  effort.  The 
patient  may  tire  more  readily  than  he  should  for  a  given 
amount  of  mental  or  bodily  exercise ;  he  is  weary  and  de- 
pressed, and  occasionally  there  is  noted  an  unusual  intol- 
erance of  alcohol  or  tobacco.  Vertigo  is  common,  especially 
on  rising  in  the  morning  or  in  suddenly  changing  from  a 
sitting  to  a  standing  position.  Some  complain  of  constant 
roaring  or  ringing  in  the  ears.  There  may  be  dull  head- 
ache that  the  accurate  fitting  of  glasses  does  not  alleviate. 
Unusual  irritability  or  somnolency  with  a  disinclination 
to  commence  a  new  task  may  be  present.  Sometimes  the 
effort  of  concentrating  the  attention  is  sufficient  to  increase 
the  headache.  This  has  been  called  ''the  sign  of- the  pain- 
ful thought."  Numbness  and  tingling  in  the  liands,  feet, 
arms,  or  legs  are  also  complained  of,  and  neuralgias,  not 
following  the  course  of  the  nerves  but  of  the  arteries,  also 
occur.  It  is  important  to  remember  that  the  train  of  symp- 
toms resembling  neurasthenia  in  a  person  over  forty-five 
years  old  may  be  due  to  incipient  arteriosclerosis.  This 
tardy  neurasthenia  frequently  accompanies  cancer,  tubercu- 
losis, diabetes,  and  incipient  general  paralysis,  as  well  as 
incipient  arteriosclerosis. 

Bleeding  from  the  nose,  epistaxis,  taking  place  frequently 
in  a  middle-aged  person,  sometimes  is  an  early  symptom. 
The  bleeding  may  be  profuse,  but  is  rarely  so  large  as  to  be 
positively  harmful.  In  fact,  it  may  do  much  good  in  reliev- 
ing tension.  Slight  edema  of  the  ankles  and  legs  is  seen. 
Dyspnea  on  slight  exertion  is  not  uncommon.  Dyspeptic 
symptoms  are  not  infrequent,  pyrosis  (heartburn),  a  feel- 
ing of  fullness  after  meals  with  belching  or  a  feeling  of 


SYMPTOMS   AND    PHYSICAL    SIGNS  185 

weight  in  the  epigastrium.  Tlie  dyspeptic  symptoms  may 
be  so  marked  that  one  might  almost  speak  of  a  variety  of 
arteriosclerosis,  the  dyspeptic  type.  For  quite  a  while  be- 
fore any  symptoms  that  would  definitely  fix  the  case  as  one 
of  undoubted  arteriosclerosis,  the  patient  complains  that 
foods  which  previously  were  digested  with  no  difficulty  now 
give  him  gastric  distress.  The  examination  of  the  stomach 
contents  of  a  patient  presenting  gastric  symptoms  reveals 
usually  a  subacidity.  The  total  acidity  measured  after  the 
Ewald  test  meal  may  be  only  20  and  the  free  HCl  may  be 
absent.  Attention  has  been  called  to  an  unnatural  pallor 
of  the  face  in  early  arteriosclerosis.  Progressive  emacia- 
tion is  sometimes  seen  in  cases  of  arteriosclerosis  and  may 
be  the  only  symptom  of  which  the  patient  complains. 

Hypertension 

Not  all  cases  of  arteriosclerosis  are  accompanied  by  in- 
creased arterial  tension.  As  has  been  stated  in  a  previous 
chapter,  the  blood  pressure  in  the  arterial  system  depends 
chiefly  on  two  factors;  viz.,  the  degree  of  peripheral  (capil- 
lary) resistance,  and  the  force  of  the  ventricular  contrac- 
tion. The  highest  arterial  pressures  recorded  with  the 
sphygmomanometer  occur  not  in  pure  arteriosclerosis  but 
in  cases  where  there  is  concomitant  chronic  interstitial  dis- 
ease of  the  kidneys.  When  this  is  found  there  is  always 
arteriosclerosis  more  or  less  marked.  In  cases  where  the 
arteries  are  so  sclerosed  that  they  feel  like  pipe  stems  there 
may  be  an  actual  decrease  in  the  blood  pressure.  Hence 
the  clinical  measuring  of  the  pressure  in  the  brachial  artery 
alone  is  not  sufficient  for  a  diagnosis  of  arteriosclerosis.  A 
persistent  high  blood  pressure  even  with  normal  urinary 
findings  is  not  a  sign  of  arteriosclerosis.  The  high  tension 
later  may  lead  to  the  production  of  sclerosis  of  the  arteries, 
but  in  these  cases  the  kidney  may  be  primarily  at  fault. 

The  impression  must  not  be  gained  that  hypertension  in 


186  ARTEUIOSCLEKOSIS 

itself  always  coiistitiites  a  disease  or  even  a  syniptoiii  of  dis- 
ease. Hypertension  itself  is  practically  always  a  compen- 
satory process.  That  is  to  say,  it  is  the  attempt  on  the  part 
of  the  body  to  equalize  the  distribution  of  blood  in  the  body 
Avhen  there  is  some  x)oison  causing  constriction  of  the  small 
arteries.  In  this  sense  hypertension  is  not  only  essential, 
but  actually  life-saving.  A  heart  which  is  so  diseased  that 
it  can  not  respond  to  the  call  for  increased  action  by  hyper- 
trophy of  its  fibers,  would  shortly  wear  out.  The  very  fact 
that  the  heart  becomes  enlarged  and  the  tension  in  the 
arteries  becomes  high,  indicates  that  in  such  a  heart  there 
was  great  reserve  power.  But  while  hypertension  is  largely 
an  effort  at  adjustment  among  the  various  parts  of  the  cir- 
culation, it  nevertheless  tends  to  increase,  provided  the 
cause  or  causes  which  produced  it  act  continuously.  More- 
over, as  has  been  said  (Chap.  II),  the  arterioles  do  not  re- 
spond to  increased  work  on  the  part  of  the  heart  by  expand- 
ing, but  by  contracting.  A  A^cious  circle  is  thus  maintained 
which  eventually  must  lead  to  serious  consequences. 

Hypertension  is  then,  if  anything,  only  a  symptom  which 
may  or  may  not  demand  treatment.  That  hypertension 
leads  to  the  production  of  sclerosis  of  the  arteries  has  been 
repeatedly  affirmed  here.  In  certain  cases  it  is  good  and 
should  not  be  experimented  with.  In  other  cases  it  is  bad 
and  some  treatment  to  reduce  the  tension  nuist  be  tried. 
The  main  point  is  to  regard  hypertension  as  one  regards  a 
compensated  heart  lesion. 

Prof.  T.  Clifford  Allbutt  divides  the  causes  of  arterio- 
sclerosis clinically  into  three  classes:  (1)  The  toxic  class — 
the  results  of  poisons  of  the  most  part  of  extrinsic  or- 
igin, chiefly  those  of  certain  infections.  In  some  of  these 
diseases,  the  blood  pressures,  as  for  example,  in  syphilis, 
are  ordinarily  unaffected ;  in  others,  as  in  lead  poisoning, 
they  are  raised.     (2)   The  class  he  calls  hyperpietic,*  in 


*Froin  TTiecrw  to  squeeze,  oppress  or  distress.     Hyperpiesis,  therefore,   signities  excessive 
pressure. 


SYMPTOMS    AXD    PHYSICAL    SIGXS  187 

Avhic'li  an  arteriosclerosis  is  tlie  consequence  of  tensile 
strength,  of  excessive  arterial  blood  pressure  persisting  for 
some  years.  A  considerable  example  of  this  class  is  the 
arteriosclerosis  of  granular  kidney,  but  in  numy  cases  kid- 
ney disease  is,  clinically  speaking,  aljsent.  (3)  The  involu- 
tionary  class,  in  which  the  change  depends  upon  a  senile,  or 
quasisenile  degradation.  This  may  be  no  more  tlian  wear 
and  tear,  a  disposition  of  all  or  of  certain  tissues  to  pre- 
mature failure — partly  atrophic,  j^c^'tly  mechanical — un- 
der ordinary  stresses;  or  it  also  may  be  toxic,  a  slow  poison- 
ing by  the  "faltering  rheums  of  age."  In  ordinary  cases 
of  this  class  the  blood  pressures  for  the  age  of  the  patient 
are  not  excessive.  Although  the  toxins  of  the  specific 
fevers,  notably  typhoid,  as  stated  above,  and  influenza,  have 
been  shown  to  produce  arteriosclerosis,  this,  under  favor- 
able circumstances  he  believes  tends  to  disaj^pear.  This 
has  been  shown  by  AViesel. 

As  the  blood  pressure  is  dependent  on  the  resistance 
offered  by  the  capillaries  and  arterioles,  there  are  only  two 
ways  in  which  increased  pressure  can  be  brought  about; 
either  by  rendering  the  blood  more  viscous,  or  by  the  gen- 
eration of  some  poison  from  the  food  taken  into  the  1)ody 
which,  acting  on  the  vasomotor  center  or  directly  on  the 
finer  vessels,  arteriolar  or  capillary,  sets  up  a  constriction 
over  any  large  area,  and  mainly  in  the  splanchnic  area.  In 
regard  to  the  liability  to  arteriosclerosis,  this  area  stands 
second  only  to  the  aortic  and  coronary  areas.  He  believes 
that  arteriosclerosis  itself  has  little  effect  in  raising  arterial 
pressure.  Many  cases  are  seen  in  which  with  extreme  ar- 
teriosclerosis there  was  no  rise  in  blood  pressure,  and  some 
in  which  pressures  have  been  rising  even  long  ])efore  the 
appearance  of  arterial  disease.  Prof.  Allbutt  also  believes 
that  in  the  hyperpietic  cases  the  arteries  undergo  a  tran- 
sient thickening,  which  can  l)e  removed  if  the  causes  can  be 
reached  and  overcome. 

Clinically  speaking,  then,  hyperpietic  arteriosclerosis  is 


1 88  ARTERIOSCLEROSIS 

not  a  disease,  but  a  meclianical  result  of  disease.  If  the  nar- 
rowing of  the  arterioles  is  brought  about  by  thickening  due 
to  arteriosclerosis,  then  it  would  seem  a  'priori  that  such 
obliteration  should  cause  a  rise  in  pressure.  Were  the 
vascular  system  a  mere  mechanical  set  of  tubes  and  a  pump, 
this  would  happen,  but  other  factors  of  great  importance 
must  be  taken  into  consideration  besides  the  meclianical 
factors;  viz.,  chemical  and  biological  factors.  Thus,  whole 
parts  may  be  closed  and  with  compensatory  dilatation  in 
other  parts  there  would  be  little  or  no  change  in  pressure, 
unless  there  were  h^^perpiesis.  In  established  hyperpiesis, 
we  note  two  conditions  in  the  radial  artery:  first,  a  compara- 
tively straight  vessel  with  a  small  diameter;  secondly,  a 
larger,  more  tortuous  vessel,  "the  large  leathery  artery." 
In  the  cases  of  the  first  group,  hyperpiesis  is  often  more 
marked,  although  not  appearing  so  to  the  examining  finger, 
than  in  the  second  class.  In  view  of  the  difficulty  of  esti- 
mating by  touch  alone  the  amount  of  hyperpiesis  in  a  con- 
tracted hard  artery,  it  is  often  overlooked  until  a  ruptured 
vessel  in  the  brain  startles  us  to  a  realization  of  our  mis- 
take. The  "narrow"  artery  is  more  dangerous  than  the 
tortuous  one,  for  w^ith  every  change  in  pressure  the  passive 
vessels  of  the  brain  must  receive  blood  that  under  normal 
conditions  would  go  to  other  parts  of  the  circulation. 

In  involutionary  sclerosis  there  is  a  gradual  thickening 
and  tortuosity  of  the  vessel,  which  although  it  may  be 
greater  than  in  the  hyperpietic  cases,  yet  is  never  so  danger- 
ous to  life.  The  heart  in  hyperpiesis  hypertrophies  and 
dilates,  but  such  a  heart  is  the  result,  not  an  integral  part, 
of  the  arterial  disease. 

The  Heart 

AVhen  the  arterial  tree  becomes  narrowed  and  the  resist- 
ance offered  to  the  flow  of  blood  thereby  is  increased,  more 
muscular  w^ork  is  required  of  the  left  ventricle  and  accord- 


SYMPTOMS    AND    PHYSICAL    SIGXS  189 

ing  to  the  general  laws  ^^ili('ll  govern  nniseles  the  ventricle 
hypertrophies.  There  is  an  actual  increase  in  number  of 
fibers  as  well  as  an  increase  in  the  size  of  the  individual 
fibers.  Some  of  the  best  examples  of  simple  hypertrophy 
of  the  left  ventricle  are  found  under  such  circumstances. 
The  chambers  as  a  rule  do  not  dilate  until  the  resistance  be- 
comes greater  than  the  contraction  can  overcome,  when 
symj^toms  of  broken  compensation  of  the  heart  take  place. 
The  hyi)ertrophy  of  the  left  ventricle  brings  more  of  this 
portion  of  the  heart  toward  the  anterior  chest  wall.  The 
enlargement  is  toward  the  left,  also,  consequently  the  apex- 
beat  is  found  below  and  to  the  left  of  its  usual  site,  even  an 
inch  or  more  beyond  the  nipjjle  line.  The  impulse  is  heav- 
ing, pushing  the  palpating  hand  forcibly  up  from  the  chest 
Avail.  The  visible  area  of  pulsation  may  occupy  three  inter- 
spaces and  the  iirecordium  is  seen  to  heave  with  every  sys- 
tole. On  auscultation  the  second  sound  at  the  aortic  carti- 
lage is  ringing,  clear,  and  accentuated.  Not  infrequently, 
too,  the  first  sound  is  loud  and  booming,  but  has  a  curious 
muffled  sound  that  may  even  be  of  a  murmurish  quality. 
The  leaflets  of  the  mitral  valve  may  be  the  seat  of  sclerosis, 
the  edges  are  slightly  thickened  and  do  not  quite  approxi- 
mate, thus  causing  a  definite  murmur  with  every  systole. 
This  murmur  may  be  transmitted  out  into  the  axilla  and  be 
heard  at  the  inferior  angle  of  the  left  scapula. 

Palpable  Arteries 

Xot  every  artery  that  can  be  felt  is  the  subject  of  arterio- 
sclerosis, and,  as  has  been  stated,  palpable  arteries  being 
more  or  less  a  condition  of  advancing  years,  judgment  as 
to  whether  the  artery  is  pathologically  or  phj'siologically 
thickened  may  be  a  matter  of  individual  opinion.  A  radial 
artery  that  lies  close  to  the  lower  end  of  the  radius  and  can 
actually  be  seen  to  pulsate  when  the  hand  is  held  slightly 
extended  on  the  back  of  the  wrist,  is  easily  felt,  but  nuist 


190  AUTERIOSCLETIOSI.S 

not,  tlicreroi'c,  1)(>  ('()iisi(l('i-(Ml  a  sclerosed  artery.  Tlie  I'adial 
may  Ix'  so  (iee])ly  situated  in  tlie  wrist  of  a  fat  sul)ject  that 
it  is  difficultly  ])alpal)lc.  Yet  the  two  cases  just  described 
may  liave  ai-teries  of  identical  structure,  there  being  no 
more  retrogressive  changes  in  the  one  than  in  the  other, 
"Experience  is  fallacious  and  judgment  difficult." 

The  small,  contracted,  wiiy  arter}^  of  a  chronic  nei)hritic 
may  feel  like  a  pipe  stem,  l)ut  if  properly  felt  the  mistake 
will  not  be  made  of  considering  such  an  artery  an  nnusually 
sclei'osed  one.  AVlien  the  wave  is  pressed  out  of  such  a 
high  tension  artery,  it  is  found  that  what  seemed  to  be  a 
iirin  sclerosed  vessel,  was  in  reality  an  artery  tightly 
stretched  ovei-  the  colunm  of  ])lood. 

Ocular  Si^s  and  Symptoms 

It  would  not  exaggerate  too  much  to  say  that  the  exami- 
nation of  the  eye  grounds  with  the  ophthalmoscoije  is  the 
most  important  aid  in  the  early  diagnosis  of  arteriosclero- 
sis. Long  before  there  are  any  subjective  symptoms, 
changes  can  be  seen  in  the  blood  vessels  of  the  retina  which, 
while  not  always  diagnostic,  at  least  call  attention  to  a  be- 
ginning chronic  disease.  As  I  become  more  proficient  in  the 
use  of  the  ophthalmoscope,  I  am  impressed  with  the  impor- 
tance of  the  ocular  signs  of  arterial  disease.  I  would  urge 
l)ractitioners  to  familiarize  themselves  with  this  instrument. 
The  electrically  lighted  insti'uments  on  the  market  now  have 
so  simplified  the  technic  that  any  ])hysician  should  be  able 
to  see  the  grosser  changes  which  take  place  in  the  arteries 
and  veins  of  the  retina  and  in  the  disc.  Frequently  the 
ophthalmologist  is  the  first  to  recognize  early  arteriosclero- 
sis. In  the  fundus  are  seen  increased  tortuosity  of  the  reti- 
nal vessels  and  their  terminal  twigs  with  more  or  less  bend- 
ing of  the  vessels  at  their  crossings.  The  arteries  are  termi- 
nal ones,  and  small  patches  of  retinitis  are  therefore  found. 
The  changes  have  been  divi<led  into  (1)  suggestive,  (2) 
pathognomonic. 


SYMPTOMS    AND    PFrVSICAL    SKJXS  191 

Under  (1)  are: 

(a)  Uneven  eali])er  of  the  vessels, 
(]))  Undue  tortuosity, 

(e)   Increased  distinctness  of  tlie  central  li^^lit  streak, 
(d)  An  unusually   lifj;-lit   color  of  tlie  breadth   of  the 
artery. 

Under  (2)  are: 

(a)  Chauf^es  in  size  and  breadth  of  the  retinal  arteries 
so  that  they  look  beaded, 

(b)  Distinct  loss  of  translucency, 

(c)  Alternate  contractions  and  dilatations  in  the  veins, 

(d)  ]\[ost  important  of  all,  the  indentation  of  the  veins 
by  the  stiffened  arteries. 

There  is  yet  another  si^i-n  which  appears  to  be  pathog-no- 
monic.  The  arteries  are  pale,  ai)pear  riftid  and  through  the 
center,  parallel  to  the  course,  is  a  rather  brift'lit,  fine  thread- 
like line.  The  appearance  is  known  as  the  ''silverwire" 
artery.  It  is  particularly  constant  in  hypertension  where 
the  most  beautiful  examples  are  seen. 

Moreover,  there  is  the  arcus  senilis,  the  fine  translucent 
to  opaque  circle  surrounding  the  outer  portion  of  the  iris. 
Practically  every  one  with  a  well-marked  arcus  senilis  has 
arteriosclerosis,  but  vice  versa  not  evei-y  one  with  even 
marked  arteriosclerosis  lias  an  arcus  senilis. 

In  general,  the  symptoms  are  gradual  loss  of  acute  vision, 
and  attacks  of  ti'ansient  loss  of  vision.  The  explanation 
which  has  been  offered  for  these  phenomena  is  the  contrac- 
tion in  a  diseased  central  artery. 

Nervous  Symptoms 

The  onset  of  arteriosclerosis  is,  in  the  majority  of  cases, 
so  insidious  that  certain  nervous  manifestations,  due  in  all 
probability  to  disturl)ances  in  l)lood  pressure,  are  ])resent 
long  before  the  actual  sclerosis  of  the  arteries  can  be  felt. 


]  92  ARTERIOSCLEROSIS 

These  nervous  syiniitoms  are  at  times  tlie  sign  posts  to  show 
us  tlie  way  to  accurate  diagnosis.  Tliere  may  be  grad- 
ual increase  in  irrital)ility  of  temjDer,  inability  to  sleep, 
vertigo  ev(Mi  extending  to  transient  attacks  of  unconscious- 
ness. Loss  of  memory  for  details  frequently  is  an  early 
symptom  of  sclei'osis  of  the  cerebral  arteries.  Nervous  in- 
digestion may  l)e  present.  Various  paresthesias  as  numb- 
ness, tingling,  a  sense  of  coldness  or  of  heat  or  burning,  a 
sense  of  stiffness  or  even  actual  stiffness  or  weakness  may 
occur  in  the  arms  and  legs,  more  frequently  in  the  legs. 
The  pain  complained  of  may  l)e  due  to  occlusion  of  an  ar- 
tery, although  evidence  for  this  is  lacking.  It  has  been 
thought  by  some  that  the  pain  in  angina  pectoris  might  be 
due  to  this  cause. 

Several  curious  and  interesting  diseases  which  have 
been  thought  by  some  to  have  arteriosclerosis  as  a  basis  are 
accompanied  by  pain.  Such  are  erythromelalgia,  Ray- 
naud's disease,  ''dead  fingers,"  and  intermittent  claudica- 
tion. 

Erb  has  reported  a  large  series  of  intermittent  limp 
(claudication)  from  his  private  practice.  He  finds  that  the 
large  majority  of  the  cases  occur  in  men.  The  abuse  of 
tobacco  was  evidently  the  main  etiologic  factor  in  about 
half  of  the  cases.  Repeated  exposure  to  cold  and  the  abuse 
of  alcohol  were  responsible  for  most  of  the  other  cases. 
Curiously  enough  he  finds  that  a  history  of  syphilis  was 
present  in  only  a  small  proportion  of  his  cases.  It  is  his 
firm  conviction  that  intermittent  limping — which  he  thinks 
should  be  called  angiosclerotic  dysbasia — is  frequently  in- 
correctly diagnosed.  It  is  mistaken  for  other  troubles  and 
treated  wrongly.  As  gangrene  may  develop  this  is  par- 
ticularly dangerous.  The  affection  generally  develops  grad- 
ually, although  he  has  seen  cases  where  the  onset  was  rather 
acute.  The  partial  or  complete  lack  of  the  pulse  in  the  foot 
is  the  one  striking  sign,  together  with  the  varying  behavior 
of  the  pulse,  its  disappearance  when  the  feet  are  cold  and 


SYMPTOMS    AND    PHYSICAL    SIGNS  193 

its  return  after  a  warm  foot  l)atli  or  under  other  treatment. 
Signs  of  general  arteriosclerosis  Avere  present  in  nearly 
every  case.  AVlien  tliere  is  a  tendency  to  tlie  development 
of  intermittent  limp  lie  tinds  that  a  valuable  sign  is  the  man- 
ner in  which  the  leg  l)lanches  when  it  is  lifted  repeatedly 
while  the  jmtient  is  recumbent  and  becomes  hyperemic  later 
when  placed  horizontally.  In  health  this  change  occurs 
more  rapidly. 


CHAPTER  IX 

SYMPTOMS  AND  PHYSICAL  SIGNS 

Special 

Our  conception  of  arteriosclerosis  as  a  degenerative  proc- 
ess affecting  the  vascular  tree  rather  than  a  disease,  re- 
moves the  possibility  of  discussing  special  symptoms.  As 
a  matter  of  fact,  we  know  of  very  few  organs  where  even 
profound  pathologic  changes  in  the  vascular  system  pro- 
duced during  life  any  symptoms  which  could  be  laid  to 
these  arterial  changes.  Kind  nature  has  given  to  us  such 
an  excess  of  organs  of  every  kind  that  the  destruction  of 
large  portions  of  any  organ  seems  to  affect  the  function 
but  little.  So  only  particular  groups  of  organs,  which  show 
symptomatic  changes  as  the  result  of  arteriosclerotic  proc- 
esses, will  be  discussed.  It  is  realized  that  this  may  not 
give  Teutonic  completeness  to  the  discussion,  but  it  cer- 
tainly saves  paper  and  has  a  distinct  practical  value  to  the 
long  suffering  reader. 

Although  arteriosclerosis  is  a  disease  which  affects  the 
whole  arterial  system,  it  nevertheless  never  reaches  the 
same  grade  all  over  the  body.  The  difference  in  the  struc- 
ture and  functions  of  the  various  organs  determines  to  great 
extent  the  eventual  symptomatology.  Endarteritis  obliter- 
ans of  a  small  sized  artery  in  the  liver  or  leg  would  lead  to 
no  marked  symptoms,  as  the  circulation  is  so  rich  that  the 
anastomoses  of  the  blood  vessels  would  soon  establish  a 
collateral  circulation  tliat  would  be  perfectly  competent  to 
sustain  the  function  of  the  part.  Quite  different  would  it 
be  should  one  of  the  small  arteries  of  the  brain,  the  lenticulo- 
striate,  for  example,  which  supplies  the  corpus  striatum, 
become  the  seat  of  a  thrombosis  or  embolism  caused  by 
arteriosclerosis.     The  arteries  of  the  brain  are  terminal 

194 


SYMPTOMS   AND   PHYSICAL    SIGNS  195 

arteries  and  the  blood  supply  would  be  cut  off  entirely  with 
a  resulting  anemic  necrosis  of  the  part  supplied  by  the 
artery  and  a  loss  of  function  of  the  part.  What  would  be 
of  no  moment  in  the  leg  or  arm  might  prove  even  fatal  in 
the  brain. 

The  further  symptomatology,  therefore,  of  arterioscle- 
rosis depends  entirely  on  the  organ  or  organs  most  affected 
by  the  interference  with  the  blood  supply.  The  following 
groups  may  be  recognized: 

1.  Cardiac. 

2.  Renal. 

3.  Abdominal. 

4.  Cerebral. 

5.  Spinal. 

6.  Local  vasomotor  effects. 

7.  Pulmonary. 

Cardiac 

Most  cases  of  arteriosclerosis  sooner  or  later  present 
symptoms  referable  to  the  heart.  When  the  organ  is  hyper- 
trophied  and  is  alread}'  working  against  an  enormous 
peripheral  resistance,  a  slight  excess  of  work  put  upon  it 
may  cause  a  dilatation  of  the  chambers  with  the  resulting 
broken  compensation.  There  is  dyspnea  on  slight  exertion, 
possibl}'  some  precordial  distress,  slight  edema  of  the  ankles 
and  lower  legs  and  possibly  scanty  urine.  With  proper 
care,  a  patient  with  such  symptoms  may  recover,  but  the 
danger  of  another  break  in  compensation  is  enhanced.  The 
next  attack  is  more  severe.  The  edema  is  greater,  there 
may  be  signs  of  edema  of  the  lungs,  effusions  into  the  serous 
cavities  may  occur.  The  heart  shows  marked  dilatation. 
There  is  gallop  or  canter  rhythm  and  there  are  loud  mur- 
murs at  the  apex.  When  a  patient  is  first  seen  in  this  stage, 
it  may  be  quite  impossible  to  state  whether  or  not  there  is 
true  valvular  disease  of  the  heart.  The  muscle  is  usually 
diseased  in  that  there  is  fibroid  degeneration  of  more  or 


196 


Ai;Tl<:itl()SCLEl!()S!S 


loss  extcMisive  chai'acter.  This  factor  causes  the  heart  to 
lose  much  of  its  elasticity  and  increases  the  tendency  to 
permanent  dilatation.  Such  cases  must  be  watched  before 
one  can  say  that  true  valvular  insufficiency  is  not  present. 
Tlie  fatal  termination  of  such  a  case  is  quite  like  that  of 


I'ig.    59. — Aneiirjsin    of    the    heart    wall.      (.Milwaukee    County    IIosi)ital.) 

true  valvular  disease.  There  is  increasing  dyspnea,  in- 
creasing anasarca,  and  the  patient  usually  succumbs  to 
edema  of  the  lungs,  drowned  in  his  own  secretions. 

A  very  rare  complication  of  the  fibroid  degeneration  of 
the  heart  nmscle  is  aneurysm  of  the  heart  wall.     (P'ig.  59.) 


SYMPTOMS    AND    PHYSICAL    SUJNS  197 

The  apex  of  the  left  ventricle  is  most  coiinnonly  the  site  of 
the  aiieiirysin  and  rupture  occasionally  occurs.  Such  an  ac- 
cident is  rapidly  fatal.  In  the  arteriosclerotic  process  which 
occurs  at  the  root  of  the  aorta,  the  coronary  arteries  become 
involved  both  at  the  openings  and  along-  the  courses  of  the 
vessels.  A  branch  or  branches  or  even  one  artery  may 
become  blocked  as  a  result  of  obliterating  endarteritis. 
The  arteries  of  the  heart  are  not  terminal  vessels  but  as  a 
rule  l)locking  of  a  lai'ge  lirancli  leads  to  anemic  infarct. 
These  areas  become  replaced  by  fibrous  tissue  which  in  the 
gross  specimen  appears  as  streaks  of  whitish  or  yellowish 
color  in  the  nmsculature.  Anemic  infarcts  may  not  occur. 
In  such  cases  the  anastomosis  bet\veen  branches  of  the  cor- 
onary arteries  is  unusually  free.  Through  arteriosclerosis 
of  the  coronary  vessels  extensive  fibrous  changes  may  oc- 
cur that  lead  to  a  myocardial  insufficiency  with  its  attend- 
ing symptoms — dyspnea,  irregular  and  intermittent  heart, 
gallop  rhythm,  edema,  etc.  One  of  the  most  distressing 
and  dangerous  results  of  sclerosis  of  the  coronary  arteries 
and  of  the  root  of  the  aorta  is  angina  pectoris.  AVliile  in 
almost  every  case  of  angina  pectoris  there  is  disease  of  the 
coronary  arteries,  the  contrary  does  not  hold  true,  for  most 
extensive  disease,  even  enil)olism,  of  the  arteries  is  fre- 
quently found  in  persons  who  never  suffered  any  attacks  of 
pain.  This  symjitom  group  is  more  connnon  in  males  than 
in  females  and  as  a  rule  occurs  only  in  adult  life.  "In  men 
under  thirty-five  svi)liilitic  aortitis  is  an  iini)ortant  factor." 
(Osier.) 

Since  the  valuable  experiments  of  Erlanger  on  heart 
block,  considera])le  attention  has  been  i)aid  to  lesions  of  the 
Y-shaped  bundle  of  fi))ers,  a  l)undle  arising  at  the  auric- 
uloventricular  node  and  extcniding  to  the  two  ventri- 
cles, known  also  as  the  auriculoventricular  bundle  of  His. 
Interference  with  the  transmission  of  imi)ulses  through  this 
bundle  gives  rise  to  the  symptom  group  known  as  the 
Stokes-Adams  svndrome,  which   is   characterized  by:    (a) 


198  ARTERIOSCLEROSIS 

slow  pulse,  (b)  cerebral  attacks — vertigo,  syncope,  tran- 
sient apoplectiform  and  epileptiform  seizures,  (c)  visible 
auricular  impulses  in  the  veins  of  the  neck.  Many  of  the 
cases  which  occur  are  in  elderly  people  the  subjects  of 
arteriosclerosis. 

So  far  as  we  now  know  all  cases  of  the  Stokes-Adams 
syndrome  are  caused  by  heart  block  which  is  only  another 


Fig.  60. — Large  aneurysiii  of  the  aorta  eroding  the  sternum.     Death  from  rupture  through 
the    .skin    preceded    by    fre(|uent    small    hemorrhages.      (Milwaukee    County    Hospital.) 

name  for  disease  in  the  auriculoventricular  bundle.  Of 
interest  here  is  the  fact  that  besides  gunmiata,  ulcers,  and 
other  lesions  of  the  bundle,  definite  arteriosclerotic  changes 
have  been  found. 

' '  The  investigation  of  a  typical  case  of  Stokes-Adams  dis- 
ease has  shown  that  the  symptoms  of  this  case  are  caused 
by  some  lesion  in  the  heart  which  gives  rise  to  the  condi- 


SYMPTOMS    AND    PHYSICAL    SIGNS  199 

tion  now  generally  termed  heart  block.  Practically  all  de- 
grees of  heart  block  have  been  observed,  namely,  complete 
heart  block  and  i^artial  block  Avith  4:1,  3:1,  and  2:1  rhythm, 
and  occasionally  ventricular  silences.  These  stages  oc- 
curred during  recovery. 

"Experiments  testing  the  reaction  of  the  heart  to  various 
extrinsic  influences  demonstrate  that  ^vhen  the  block  is  com- 
plete the  ventricles  do  not  respond  to  influences  presumably 
of  vagus  origin,  although  the  auricles  still  respond  nor- 
mally to  such  influences,  that  effects  exerted  upon  the  heart 
presumably  through  the  accelerators  still  influence  the  rate 
of  the  ventricles  as  well  as  that  of  the  auricles. 

"When  the  block  is  jjartial  the  rate  of  the  ventricular  con- 
traction varies  proportionally  with  the  rate  of  the  auricular 
contractions  but  only  within  certain  limits.  When  these 
limits  are  exceeded  the  block  becomes  more  complete,  i.  e., 
a  2:1  rhythm  may  be  changed  into  a  3:1  rhythm,  this  into 
a  4:1  rhythm,  and  this  into  complete  block,  and  vice  versa. 

"The  syncopal  attacks  are,  in  all  probability,  directly  de- 
pendent upon  a  marked  reduction  of  the  ventricular  rate. 
Such  reductions  of  the  ventricular  rate  are  always  asso- 
ciated with  an  increase  of  the  auricular  rate,  and  it  is 
believed  that  the  latter  is  the  cause  of  the  former."  (Er- 
langer.) 

The  epileptifonn  seizures  of  the  syndrome  may  be  caused 
by  the  anemia  of  the  brain  resulting  from  failure  of  the 
heart  to  supply  a  sufficient  quantity  of  blood. 

The  apoplectiform  attacks  are  most  probably  caused  by 
venous  congestion  when  the  slowing  of  the  ventricular  con- 
tractions is  not  sufficient  to  cause  convulsions,  but  will  just 
cause  complete  unconsciousness. 

Renal 

Chronic  nephritis,  hypertension,  arteriosclerosis  form  a 
most  important  trinity.  Some  stoutly  affirm  that  in  all 
cases  of  high  tension  there  is  chronic  renal  disease.     Cer- 


lM)()  AHTE1U08CLEUO.SIS 

taiiily  the  very  liigliest  blood  i)ressures  wliicli  we  see  occur 
m  the  chronic  interstitial  forms  of  kidney  disease.  The 
cause  is  most  proTjabl^'  to  be  sought  in  some  poison  Avhich 
is  elal)orated  in  the  kidney,  is  a])sorbed  into  the  circula- 
tion and  acts  powerfully  either  on  the  vasoconstrictor  cen- 
ter as  a  stimulus,  or  directly  on  the  musculature  of  the 
small  arteries  all  over  the  body.  Usually  hypertension  is 
])rogressive  but  it  may  be  temporary. 

A  man,  43  years  old,  entered  the  Milwaukee  County  Hos- 
pital in  uremic  coma.  The  systolic  blood  pressure  was 
280-1^90  mm.  llg,  the  diastolic  pressure  220  nun.  ( Janeway 
instrument).  Under  treatment  his  blood  pressure  gradu- 
ally became  lower,  at  the  same  period  the  albumin  and 
casts  gradually  disappeared  from  the  urine.  In  two  weeks 
from  admission  he  seemed  perfectly  well,  there  Avere  no 
albumin  or  casts  found  in  the  urine,  and  the  systolic  blood 
pressure  was  136  mm.,  not  a  high  tigure  for  a  muscular  man 
of  the  laboring  class.  It  must  be  admitted,  however,  that 
such  cases  are  the  exception,  not  the  rule. 

Patients  suffering  from  the  association  of  chronic  nephri- 
tis with  hypertension  die  slowly,  usualh\  There  is  gradual 
development  of  anasarca.  Headache  is  frequent  and 
severe.  Pains  all  over  the  body  may  occur.  The  sight 
may  suddenly  become  dim  or  may  even  be  lost.  Dizziness 
may  be  complained  of  and  dyspnea  is  usually  marked. 
Cyanosis  comes  on,  the  pulse  becomes  weak,  irregular  or 
intermittent,  heart  failure  sets  in,  and  the  patient  dies  with 
edema  of  the  lungs. 

Another  class  of  renal  arteriosclerosis  is  characterized 
by  a  small  granular  kidney  in  which  fibrous  changes  of  a 
patchy  character  have  taken  place.  These  scattered  areas 
are  the  result  of  obliterating  endarteritis  of  renal  arteries 
here  and  there  with  consequent  anemia,  death  of  cells,  and 
replacement  by  fibrous  tissue.  It  occurs  as  part  of  a  gen- 
eralized arteriosclerosis  in  which  the  whole  arterial  system 
is  the  seat  of  diffuse  (senile)  sclerosis.     The  palpable  ar- 


SYMPTOMS   AND    PHYSICAL    SIGNS  201 

teries  are  usually  beaded  or  even  encircled  with  calcareous 
deposits  and  the  aorta  is  the  seat  of  an  extensive  nodular 
and  ulcerating  sclerosis.  The  heart  is  usually  small,  shows 
extensive  fibrous  and  fatty  changes  and  possibly  the  condi- 
tion known  as  ''brown  atrophy;"  the  blood  pressure  is  low. 
Such  cases  do  not  show  any  special  symptoms.  They  are 
anemic,  short  of  breath  on  exertion,  have  the  appearance 
and  show  the  signs  of  senility. 

In  the  first  grouj)  it  is,  at  times,  difficult  to  say  whether 
the  kidney  disease  or  the  arterial  disease  is  the  most  im- 
portant. From  a  clinical  standpoint  the  decision  is  not 
essential  as  the  end  results  are  much  the  same  in  both. 
However,  when  actual  uremic  symptoms  dominate  the 
picture,  it  becomes  evident  that  the  disease  of  the  kidney  is 
the  chief  feature  in  the  causation  of  the  symptoms. 

Abdominal  or  Visceral 

Tbere  is  an  important  group  of  cases  to  which  but  little 
attention  has  been  paid  until  quite  recently.  This  is  the 
abdominal  or  visceral  type  of  arteriosclerosis.  It  has  been 
stated  that  arteriosclerosis  of  the  splanchnic  vessels  almost 
invariably  causes  high  tension.  Among  others,  Janeway 
has  shown  that  general  arteriosclerosis  without  marked 
disease  of  the  splanchnic  vessels  does  not  cause  as  a  rule 
increase  of  blood  pressure. 

There  are  cases  in  which  the  brunt  of  the  lesion  falls  upon 
the  abdominal  vessels.  Such  cases  have  been  called 
''angina  abdominalis."  It  has  been  suggested  (Harlow 
Brooks)  that  this  type  of  arteriosclerosis  may  be  deter- 
mined by  constant  overloading  of  the  stomach  with  food, 
especially  rich  and  spiced  food.  This  causes  overwork  of 
the  special  arteries  connected  with  digestion  and  so  leads 
to  sclerosis  of  the  vessels  of  the  stomach,  pancreas,  and  in- 
testines. Personal  habits  probably  influence  to  great  ex- 
tent the  production  of  this  more  or  less  localized  condition. 

The  organs  supplied  by  the  diseased  arteries  suffer  from 


202  AKTERIOSCLEROSIS 

clianges  analogous  to  those  occurring  in  general  or  local 
malnutrition,  such  as  starvation,  old  age,  or  local  anemias. 
These  changes  are  atrophy  with  hemachromatosis  (brown 
atrophy)  or  fatty  infiltration  and  degeneration.  Following 
the  degenerative  changes  there  result  connective  tissue 
growth  and  further  limitation  of  the  functionating  power  of 
the  affected  organs. 

Pain  is  a  more  or  less  constant  symptom  of  visceral 
sclerosis.  In  the  early  stages  there  may  be  only  a  sense 
of  oppression,  of  weight,  or  of  actual  pressure  in  the  abdo- 
men or  pit  of  the  stomach.  There  may  be  only  recurring 
attacks  of  violent  abdominal  pain  accompanied  by  vomiting. 
In  some  cases  symptoms  of  tenderness  in  the  epigastrium, 
pains  in  the  stomach  after  eating,  vomiting  and  backache 
may  suggest  gastric  ulcer.  There  may  be  dyspnea  and  a 
sense  of  anguish  accompanied  with  a  rapid  and  feeble  pulse, 
Hematemesis  may  make  the  symptom  group  even  more  like 
ulcer  of  the  stomach,  and  only  the  course  of  the  disease 
with  the  failure  of  rigid  ulcer  treatment  and  the  substitu- 
tion of  treatment  directed  toward  relief  of  the  arterial 
spasm  with  resulting  betterment,  enables  one  to  make  a 
diagnosis.  The  condition  may  be  present  for  years  and  the 
symptoms  only  epigastric  tenderness  with  dizziness  and 
sweating  on  lying  down  after  dinner,  as  in  one  of  Perutz's 
patients.  The  attacks  are  probably  due  to  spasmodic  con- 
traction of  the  sclerosed  intestinal  vessels  with  a  resulting 
local  rise  in  blood  pressure.  The  pains  are  most  probably 
due  to  the  spasm  of  the  intestinal  muscles,  and  some  think 
they  are  located  in  the  sympathetic  and  mesenteric  plexuses. 

This  result  of  arteriosclerosis  is  not  so  uncommon,  and 
by  keeping  this  cause  of  obscure  abdominal  pain  in  mind 
we  are  now  and  then  enabled  to  save  a  patient  from  opera- 
tion. 

An  autopsy  on  a  case  which  for  many  years  had  attacks 
of  abdominal  pain  and  cramp-like  attacks,  with  high  blood 
pressure  and  heart  hypertrophy,  showed  extensive  sclerosis 


SYMPTOMS   AND    PHYSICAL    SIGNS  203 

of  the  abdominal  aorta,  superior  mesenteric  and  iliacs. 
These  vessels  were  calcified.  Hypertrophy  of  the  left 
ventricle  was  found.  The  kidneys  were  microscopically 
normal.  There  were  no  changes  in  the  ascending  aorta  but 
in  the  descending  portion  there  were  scattered  nodules  and 
small  calcified  plaques. 

The  attacks  of  pain  from  which  this  patient  suffered  for 
many  years,  the  hypertrophy  of  the  left  ventricle  and  the 
increased  blood  pressure  were  thought  to  be  directly  due 
to  the  sclerosis  of  the  abdominal  vessels. 

Cerebral 

It  has  been  stated  tliat  arteriosckn'osis  is  a  general  dis- 
ease, yet  certain  systems  of  vessels  may  l)e  affected  far 
more  than  others,  and  indeed  there  may  be  marked  sclerosis 
at  one  part  of  tlie  body  and  none  demonstrable  at  another 
part. 

In  advanced  sclerosis  there  may  be  one  or  more  of  a  series 
of  accidents  due  to  embolism,  thrombosis,  or  rupture  of  the 
vessels.  Such  conditions  as  transient  hemiplegia,  mono- 
plegia or  aphasia  may  occur.  The  attacks  may  come  on 
suddenly  and  be  over  in  a  few  minutes;  what  Allbutt  calls 
"Larval  apoplexies."  They  may  last  from  a  few  hours 
up  to  a  day,  and  are  very  characteristic.  A  patient  aged 
64  years  with  pipe  stem  radials  and  tortuous  hard  temporals 
would  be  lying  quietly  in  bed  when  suddenly  he  would 
stiffen,  the  eyes  would  become  fixed  and  the  breathing 
cease.  In  a  few  seconds  consciousness  returned,  the  patient 
would  shake  himself,  pass  his  hand  over  his  brow  and  ask, 
''Where  am  I?  Oh,  yes,  that's  all  right."  He  had  as  many 
as  thirty  of  these  attacks  in  twenty-four  hours,  none  of 
them  lasting  over  one  minute.  To  just  Avhat  such  attacks 
are  due,  it  is  hard  to  say.  Some  have  attributed  them  to 
spasm  of  the  smaller  blood  vessels  of  the  brain,  but  there 
have  never  been  demonstrated  in  the  vessels  any  constrictor 
fibers. 


204  AltTEItlOSCLEIlOSlS 

Tliore  is  a  well  recognized  form  of  deiiientia  caused  by 
arteriosclerosis.  In  ^'eiieral  ])aralysis  of  tlie  insane  and 
in  senile  dementia  the  blood  vessels  are  always  diseased. 
Milder  grades  of  i)sycliic  disturbances  are  accomjoanied  by 
such  symi)toms  as  inental  fatigue,  j^^'i'^^i^tent  lieadaclies, 
vertigo,  memory  weakness  and  fainting.  Apliasia,  j)eriods 
of  excitement  and  mental  confusion  occur  in  some.  Later 
stages  are  at  times  accompanied  by  inclination  to  fabulate, 
loss  of  judgment,  disorientation,  narrowing  of  the  external 
interests,  episodes  of  confusion  and  hallucinatory  delirium. 

The  hemiplegias,  monoplegias  and  paraplegias  may  oc- 
cur again  and  again  and  last  for  one  or  two  days.  Unless 
there  has  been  rui)ture  of  the  vessels,  there  is  complete  re- 
covery as  a  rule. 

In  persons  who  have  arteriosclerosis  with  high  tension 
attacks  of  melancholia  are  seen.  There  are  at  the  same 
time  fits  of  depression,  insomnia,  irritability,  fretfulness, 
and  a  generally  marked  change  in  disposition.  AVhen  the 
tension  is  reduced  by  appropriate  treatment  these  symjj- 
toms  disappear,  to  recur  when  the  tension  again  becomes 
high.  On  the  contrary,  attacks  of  mania  are  accompanied 
by  low  blood  jjressure.  The  dizziness  and  vertigo  in  cere- 
bral arteriosclerosis  are  probably  due  to  the  stiffness  of  the 
vessels  which  prevents  them  from  following  closely  the  va- 
riations of  pressure  jn'oduced  by  position,  and  thus,  at 
times,  the  brain  is  deprived  of  l)lood  and  a  transient  anemia 
occurs. 

Arteriosclerosis  of  the  cei-ebral  vessels  is  always  a  seri- 
ous condition.  The  greatest  danger  is  from  rupture  of  a 
l)lo()d  vessel.  Another  of  the  dangei's  is  gradual  occlusion 
of  the  arteries  bringing  about  necrosis  with  softening  of  the 
brain  substance.  The  latter  is  more  apt  to  be  associated 
with  psychic  changes,  dementia,  etc.;  the  foi-mer,  with 
hemiplegia.  It  is  curious  that  a  small  branch  of  the  Sylvian 
artery,  the  lenticulo-striate,  which  supplies  the  corpus  stria- 
tum, should  be  the  one  which  most  frequently  ruptures. 


SYMPTOMS    AND    PHYSICAL    SIGNS  20o 

AVliere  tlio  motor  fibors  fi-oiii  tlie  wliolo  cortex  arc  <>atlici'c(l 
toft'etlier  in  one  coiii])act  bundle,  a  very  small  licmorrlia^e 
may  and  does  cause  very  serious  effects.  A  com])ai'atively 
large  hemorrliage  in  tlie  silent  area  of  the  l)rain  may  cause 
few  or  no  symjitoms. 

Spinal 

It  is  conceivable  that  arteriosclerosis  of  the  vessels  of 
the  sijinal  cord  might  cause  symptoms  which  would  be  re- 
ferred to  the  areas  of  the  cord  where  the  process  was  most 
advanced.  The  lesions  would  be  scattered  and  conse- 
quently the  symptoms  might  be  protean  in  character. 

True  ei)ileptic  convidsions  dependent  on  arteriosclerotic 
changes  are  also  seen  and  are  not  so  uncommon. 

This  is  on  the  whole  a  rare  condition,  much  less  common 
than  arteriosclerosis  of  the  cerebral  vessels.  Collins  and 
Zabriskie  report  the  following  tyj^ical  case: 

"H.,  a  fireman,  fifty-one  years  old,  Avas  in  oixlinary  good  health  until  to- 
ward the  end  of  1902.  At  that  time  he  noticed  that  his  legs  were  growing 
weak  and  that  they  tired  easily.  Later  he  complained  of  a  jerking  sensation 
iu  different  parts  of  the  lower  extremities  and  at  times  of  sharp  pain,  Avhich 
might  last  from  several  minutes  to  two  or  three  hours.  The  legs  were  the 
seat  of  a  heavy,  uuAvieldy  sensation,  but  there  Avas  no  numbness  or  other 
paresthesia.  About  the  same  time  he  began  to  have  difiiculty  in  holding  the 
urine,  a  symptom  which  steadily  increased  in  severity.  These  symptoms  con- 
tinued until  March,  1903,  i.  e.,  for  three  months,  then  he  awakened  one  morn- 
ing to  find  that  he  was  unable  to  stand  or  walk,  and  the  sphincters  of  the 
bowels  and  bladder  relaxed.  There  was  no  complaint  of  pain  in  the  back  or 
legs,  no  diflfieulty  in  moving  the  arms,  in  swallowing  or  in  speaking.  He  says 
he  was  able  to  tell  when  his  lower  extremities  were  touched  and  he  could 
feel  the  bed  and  clothes.  He  was  admitted  to  the  City  Hospital  three  Aveeks 
later  and  the  following  record  was  made  on  April  21,  190.'?. 

"The  patient  was  a  frail,  emaciated  man  of  medium  height,  Avho  had  the 
appearance  of  being  55-60  years  of  age.  He  was  unable  to  stand  or  walk. 
When  he  Avas  lying,  he  could  flex  the  thigh  and  the  legs  slowly  and  feebly. 
There  Avas  slight  atrophy  of  the  anterior  and  inner  muscles,  more  of  the  left 
than  of  the  right  side.  The  knee  jerks  and  ankle  jerks  Avere  absent.  Irri- 
tation of  the  soles  caused  cpiite  a  typical  Babinski  jihenomenon.  The  i)atient 
had  fair  strength  in  the  upper  extremities,  but  the  arms  tired  very  soon,  ho 
said.  The  grip  i^-as  moderate  and  alike  in  each  hand.  The  motility  of  the 
face,  head,  and  neck  was  not   noticeably   impaired.     There   Avas   no   difliculty 


206  APtTEPJOSCLEROSTS 

ill  swallowinjif,  aiiA  articulation  was  not  defective.  Tactile  sensibility  was 
slightly  disordered  in  the  lower  extremities,  although  he  could  feel  contact  of 
the  finger,  the  point  of  a  pin,  and  the  like.  .Sensibility  was  not  so  acute  as 
normal;  there  was  a  quantitative  diminution.  Sensory  perception  was  not 
delayed.  There  was  a  distinct  zone  of  slight  hyperesthesia  about  as  wide  as 
the  hand  above  the  femoral  trochanters.  Above  that,  sensibility  was  normal. 
There  was  no  discernible  impairment  of  thermal  sensibility.  No  part  of  the 
body  was  jiartieularly  tender  on  pressure.  A  bedsore  existed  over  the  sacrum, 
and  there  was  excoriation  of  the  genitals  from  constant  dribbling  of  urine. 

' '  Examination  of  the  chest  showed  shallow  respiratory  movements.  The 
heart  was  regular,  weak,  there  were  no  murmurs,  the  second  sound  was  ac- 
centuated. Examination  of  the  abdomen  showed  that  the  liver  and  spleen 
were  palpable,  but  were  not  enlarged.  The  abdominal  reflexes,  both  upper  and 
lower,  Avere  sluggish.  The  patient  was  slow  of  speech,  likewise  apparently  of 
thought.  He  did  not  seem  to  show  an  adequate  interest  in  his  condition,  still 
he  was  fully  oriented  and  seemed  to  have  a  fair  memory.  His  mental  reflex 
was  slow.  There  were  indications  in  the  peripheral  blood  vessels  and  heart  of 
a  moderate  degree  of  general  arteriosclerosis.  The  peripheral  vessels 
such  as  the  radial,  were  palpable,  the  walls  thickened,  the  blood  pressure 
increased. 

' '  The  patient  did  not  complain  of  pain  while  he  was  in  the  hospital,  a 
period  of  four  weeks,  nor  was  there  any  particular  change  in  the  patient's 
symptoms,  subjective  and  objective,  during  this  time.  His  mental  state  re- 
mained clear  until  forty-eight  hours  before  death,  when  ho  became  sleepy, 
stuporous,  and  comatose,  dying  apparently  of  cardiac  weakness,  which  had  set 
in  simultaneously  with  the  clouding  of  consciousness. ' ' 

At  autopsy,  except  for  a  few  small  hemorrhages  in  the  posterior  horns  of 
the  lower  dorsal  segments  on  the  right  side  and  a  similar  condition  of  the  left 
anterior  horns,  there  was  nothing  noticed.  On  microscopic  examination,  there 
was  found  widespread  sclerosis  of  the  vessels  of  the  cord  to  a  marked  degree 
with  only  slight  thickening  of  the  vessels  of  the  brain.  There  were  secondary 
degenerations  of  ascending  and  descending  type  particularly  marked  at  the 
ninth  dorsal  segment.  They  included  portions  of  all  the  tracts,  the  pyramidal 
tract  as  well.  The  symptoms  in  brief  were:  (1)  weakness  and  easily  induced 
fatigue  of  the  legs;  (2)  peculiar  sensations  in  the  lower  extremities,  de- 
scribed as  jerky,  numbness,  heaviness,  and  occasionally  sharp  pain;  (3) 
progressive  incontinence  of  iirine;    (4)   progressive  paraplegia. 

Since  one  of  tlie  cliief  manifestations  of  syphilis  is  sclero- 
sis of  the  arteries,  neurologic  cases  characterized  by  irregu- 
lar symptoms  and  signs  which  can  not  be  placed  in  any  of 
the  definite  system  disease  groups,  are  possibly  due  to 
irregularly  scattered  areas  of  sclerosis  throughout  the 
spinal  cord  caused  by  obliterating  arteritis.  Such  cases 
are  not  so  very  uncommon.    Several  have  come  under  my 


SYMPTOMS    AND    PHYSICAL    SIGNS  207 

observation.  Further  studies  of  tlie  spinal  cords  of  tliese 
cases  at  autopsy  are  necessary  before  a  final  opinion  can 
be  given  as  to  their  dependence  on  arteriosclerosis  of  the 
spinal  vessels. 

Local  or  Peripheral 

When  the  arteriosclerosis  in  the  peripheral  arteries 
reaches  a  stage  where  endarteritis  obliterans  supervenes, 
there  is  usually  no  chance  for  a  compensatory  or  collateral 
circulation  to  be  established.  The  area  supplied  by  the  ves- 
sel undergoes  dry  gangrene.  A  portion  of  a  toe  or  finger  or 
a  Avliole  foot  or  hand  may  shrivel  up.  It  is  more  common  to 
see  the  spontaneous  amputation  take  place  in  the  lower  ex- 
tremities. The  same  effect  may  be  produced  by  the  plug- 
ging of  a  vessel  with  a  thrombus.  There  may  be  much  pain 
connected  Avith  the  sudden  blocking,  whereas  tlie  gradual 
obliteration  of  the  blood  supply  of  a  toe  or  foot  is  not  as  a 
rule  at  all  painful.  The  condition  is  at  times  revealed  more 
or  less  accidentally  when  a  patient  injures  his  toe  or  foot 
and  discovers  that  there  is  no  sensation  in  the  part  and  that 
the  wound  instead  of  liealing  is  inclined  to  grow  larger. 

Other  interesting  vasomotor  j^henomena  are  frequently 
connected  with  arteriosclerosis.  Such  a  one  is  the  curious 
condition  knoA\Ti  as  Kaynaud's  disease,  a  vascular  disorder 
which  is  divided  into  three  grades  of  intensity:  (1)  local 
syncope,  (2)  local  asphyxia,  (3)  local  or  symmetrical  gan- 
grene. This  is  not  the  place  to  describe  this  condition  ex- 
cept to  say  that  the  condition  called  "dead  fingers"  is  the 
most  characteristic  feature  of  the  first  stage.  Chilblains 
represent  the  mildest  grade  of  the  second  stage.  The  parts 
are  intensely  congested  and  there  may  be  excruciating  pain. 
Any  one  who  has  ever  had  chil))lains  knows  how  painful 
they  can  be.  The  general  health  is  not  impaired  as  a  rule, 
although  the  attacks  are  apt  to  come  on  when  the  person  is 
run  down.     The  third  stage  may  vary  from  a  very  mild 


208  ARTERIOSCLEROSIS 

f>i"ado,  M'itli  only  small  necrotic  areas  at  tlie  ti])s  of  tlie 
fingers,  to  extensive  multiple  gangrene. 

Another  and  very  rare  condition  in  wliicli  clironic  endar- 
teritis Avas  the  only  constant  finding  is  the  disease  described 
by  S.  AVeir  Mitchell  and  called  by  him  erythromelalgia  (I'ed 
neuralgia).  This  is  ''A  clironic  disease  in  which  a  part  or 
parts — usually  one  or  more  extremities — suffer  with  pain, 
Hushing,  and  local  fever,  made  far  worse  if  the  parts  hang 
doAvn."     (Weir  Mitchell.) 

Probal)ly  the  most  frequently  seen  result  of  arteriosclero- 
sis in  the  leg  arteries  is  the  remarkable  condition,  first  de- 
scribed by  Charcot,  known  as  intermittent  claudication. 
Persons  the  subject  of  this  disease  are  able  to  walk  if  they 
go  slowly.  If,  however,  any  attempt  be  made  to  hurry  the 
step,  there  results  total  disability  accompanied  at  times  by 
consideral)le  cramp-like  pain.  The  condition  is  much  more 
prone  to  occur  in  men  than  in  women,  and  Hebrews  seem 
more  frequently  affected.  The  cause  is  most  probably  to 
be  sought  in  the  anemia  which  results  from  the  narrowing 
of  the  channels  through  Avhich  the  blood  reaches  the  part. 
The  stiff,  much  narrowed  arteries  allow  sufficient  blood  to 
pass  along  for  the  nutrition  of  the  part  at  rest  or  in  quiet 
motion.  Just  as  soon  as  more  violent  exercise  is  taken, 
calling  for  more  blood,  an  ischemia  of  the  part  supervenes, 
for  the  stiff  vessels  can  not  accommodate  themselves  to 
changes  in  the  necessary  vascularity  of  the  part.  A  rest 
brings  about  a  gradual  return  of  blood  and  the  function  of 
the  part  is  restored.  Pulsation  may  be  totally  absent  in  the 
dorsal  arteries  of  tlie  feet  and  when  the  legs  are  allowed  to 
hang  down  there  is  apt  to  be  deep  congestion. 

In  this  connection  a  curious  case  reported  by  Parkes 
AVeber  will  not  be  out  of  place.  The  patient,  a  male,  aged 
42  years,  complained  of  cramp-like  pains  in  the  sole  of  the 
left  foot  and  calf  of  the  leg  occurring  after  walking  for  a 
feAv  minutes  and  obliging  him  to  rest  frequently.  AA'lien 
the  legs  were  alloAved  to  hang  over  the  side  of  the  bed,  the 


SYMPTOMS    AND    PIFYSICAL    SIGNS  209 

distal  i)oi"tion  of  tlie  left  foot  became  red  and  ('Oii<>;ested 
lookiiit;-,  Xo  pulsation  conld  l)e  felt  in  the  dorsal  artery  of 
the  left  foot  or  in  the  posterior  tibial  artery.  There  Avas  no 
evidence  of  cardiovascular  or  other  disease.  An  ulcer  on 
the  little  toe  had  slowly  healed,  but  cramp-like  muscular 
pains  still  occurred  on  walkinf!,-.  The  disease  had  lasted 
about  five  years  without  the  appearance  of  fi,'an.c,i-ene. 

AVeber  calls  this  case  one  of  arteritis  obliterans  with  in- 
termittent claudication. 

Pulmonary  Artery 

In  the  symptomatolo,i;y  of  sclerosis  of  the  ])ulmonary 
artery  the  clinical  signs  and  symptoms  are  mostly  referable 
to  the  obliterating  endarteritis  of  the  smaller  vessels,  while 
the  ])hysical  signs  are  more  apt  to  reveal  the  involvement  of 
the  main  trunk.  A  history  of  severe  infection  in  the  past 
is  frequent,  especially  smallpox,  and  accompanying  aortic 
sclerosis  with  insufficiency  of  the  mitral  valve  or  stenosis  of 
this  valve  is  the  rule.  Striking  cyanosis  is  an  early  symp- 
tom, while  there  is  little  if  any  dyspnea  and  edema.  Inter- 
mittent dyspragia  is  common.  There  seems  to  be  no 
tendency  to  clubbed  fingers.  Repeated  hemorrhages  from 
the  lungs  without  the  formation  of  infarcts  may  occur. 
There  is  usually  an  area  of  dullness  at  the  upper  left  mar- 
gin of  the  sternum  and  nearby  parts,  sensitive  to  pressure 
and  to  percussion,  and  the  heart  dullness  extends  unusually 
far  towards  the  right.  The  diagiu)sis  of  the  right  ventricu- 
lar hypertrophy  may  be  substantiated  by  a  fluoroscopic  ex- 
amination. 


CHAPTER  X 
DIAGNOSIS 

Early  Diagnosis 

Arteriosclerosis  is  essentially  a  disease  of  middle  life 
and  old  age.  It  is  not  unusual,  however,  to  find  evi- 
dences of  the  disease  in  persons  in  the  third  decade  and 
even  in  the  second  decade.  Hereditary  influences  play 
a  most  important  role,  syphilis  and  the  abuse  of  alcohol 
in  the  family  history  are  particularly  momentous.  The 
recognition  of  the  early  changes  in  the  arteries  among 
young  persons  depends  largely  upon  how  carefully  these 
changes  are  looked  for.  The  difference  in  the  point  of  view 
of  one  man  who  finds  many  cases  in  the  comparatively 
young,  and  another  man  who  rarely  finds  such  changes  early 
in  life,  at  times,  depends  upon  the  acuity  of  perception  and 
observation  and  not  upon  the  fact  that  one  man  has  had  a 
series  of  unusually  young  arteriosclerotic  subjects.  The 
diagnosis  of  arteriosclerosis  may  be  so  easily  made  that  the 
tyro  could  not  fail  to  make  it.  It  is,  however,  the  purpose 
of  this  volume  to  lay  stress  on  the  earliest  possible  diagnosis 
and,  if  possible,  to  point  out  how  the  diagnosis  may  be  ar- 
rived at.  It  is  obviously  much  to  the  advantage  of  the  pa- 
tient to  know  that  certain  changes  are  beginning  in  his 
arteries,  which,  if  allowed  to  go  on,  will  inevitably  lead  to 
one  or  more  of  the  symptom  groups  described  in  the  pre- 
ceding chapters. 

The  combination  of  (1)  hypertrophied  heart,  (2)  in- 
creased blood  pressure,  (3)  palpal)le  arteries,  and  (4) 
ringing,  accentuated  second  sound  at  the  aortic  cartilage  is, 
in  reality,  the  picture  of  advanced  arteriosclerosis.  If  the 
individual  is  in  good  condition  much  may  be  done  by  judi- 

210 


DTAGXOSTS  211 

cious  advice  and  treatment  to  ward  off  complications  and 
prolong  life  with  a  considerable  degree  of  comfort.  But  we 
should  not  wait  until  such  signs  are  found  before  making  a 
diagnosis  and  instituting  treatment.  As  in  all  forms  of 
chronic  disease  the  early  diagnosis  is  all  important. 

The  history  of  the  case  is  the  first  essential.  Often  a  care- 
ful inquiry  into  the  personal  habits  of  a  patient,  with  the 
record  of  all  the  preceding  infectious  diseases  will  give  us 
valuable  information  and  may  be  the  means  of  directing  the 
attention  at  once  to  the  possible  true  condition.  Particu- 
larly must  we  inquire  into  the  family  history  of  gout  and 
rheumatism.  An  individual  who  comes  of  gouty  stock  is 
certainly  more  prone  to  arterial  degeneration  than  one  who 
can  show  a  healthy  heredity.  Alcoholism  in  the  family  also 
is  of  importance  because  of  the  fact  that  the  children  of 
alcoholics  start  in  life  with  a  poor  quality  of  tissue,  and 
conditions  that  would  not  affect  a  man  from  healthy  stock 
might  cause  early  degeneration  of  arterial  tissue  in  one  of 
l)ad  ancestry. 

What  infectious  diseases  has  the  patient  had  ?  Even  the 
exanthemata  may  cause  degenerations  in  the  arteries,  but, 
as  has  been  shown,  such  lesions  probably  heal  completely 
with  no  resulting  damage  to  the  vessel.  Should  the  patient 
have  passed  through  a  long  siege  of  typhoid  fever  the  prob- 
lem is  quite  different.  Here  (vide  supra)  (Thayer),  the 
palpable  arteries  do  appear  to  be  sclerosed  permanently. 
Probably  the  length  of  time  that  the  toxin  has  had  a  chance 
to  act  determines  the  permanent  damage  to  the  vessel  wall. 
More  potent  than  all  other  diseases  to  cause  earh'  arterio- 
sclerosis is  syphilis,  and  hence  very  careful  inquiry  should 
be  made  in  regard  to  the  possibility  of  infection  with  this 
virus.  Not  only  the  fact  of  actual  infection  but  the  dura- 
tion and  thoroughness  of  treatment  are  important  matters 
for  the  physician  to  know. 

What  is  the  patient's  occupation?  Has  he  been  an 
athlete,  particularly  an  oarsman?    Has  he  been  under  any 


21 2  ARTKItlOSCLEltOSlS 

sovero,  i)r()l()n*ie(l,  mental  strain.'  Is  he  a  laborer?  If  so, 
in  what  form  of  manual  labor  is  he  en^'aged  ?  Such  ques- 
tions as  these  should  never  be  overlooked,  as  they  form  the 
foundation  stones  of  an  accurate  diagnosis,  and  early,  ac- 
curate diagnosis,  we  repeat,  is  essential  to  successful 
therapy. 

We  have  called  attention  to  the  factor  of  sustained  high 
pressure  in  the  production  of  arteriosclerosis.  Constant 
overstretching  of  the  vessels  leads  to  efforts  of  the  body  to 
increase  the  strength  of  the  part  or  parts.  The  material 
which  is  used  to  strengthen  the  weakened  walls  has  a  higher 
elastic  resistance  than  muscle  and  elastic  tissue,  but  a  lower 
limit  of  elasticity,  and  is  none  other  than  the  familiar  con- 
nective tissue.  In  athletes,  laborers,  brain  workers  who  are 
under  constant  mental  strain,  and  in  those  whose  calling 
brings  them  into  contact  with  such  poisons  as  lead,  there  is 
every  factor  necessary  for  the  production  of  high  tension 
and  consequently  of  arteriosclerosis. 

Another  question  in  regard  to  personal  habits  is  how 
much  tobacco  does  the  patient  use  and  in  .what  form  does  he 
use  it  ?  Our  experience  is  that  the  cigar  smoker  is  more 
prone  to  present  the  symptoms  of  arteriosclerosis  than  the 
cigarette  smoker,  the  pipe  smoker,  or  the  one  who  chews  the 
tobacco.  A  very  irritable  heart  results  not  infrequently 
from  cigarette  smoking  but  such  is  almost  always  found  in 
young  men  in  whom  the  lesions  of  arteriosclerosis  are  ex- 
ceedingly rare.  The  probal)ilities  are  that  the  arterioscle- 
rosis in  cigar  smoking  results  from  the  slowly  acting  poison 
which  causes  a  rapid  heart  rate  with  an  increase  of  pressure. 

Last  but  not  least,  and  perhaps  the  most  important  ques- 
tion is,  has  the  patient  been  a  heavy  eater?  This  I  believe 
to  be  a  potent  cause  of  splanchnic  arteriosclerosis  with  the 
resulting  indigestion,  cramp-like  attacks,  high  blood  pres- 
sure, etc.  In  a  joking  manner  we  are  accustomed  to  re- 
mark, '^ Overeating  is  the  curse  of  the  American  people." 
There  is,  however,  much  truth  in  that  sentence.    Osier,  than 


DIAGNOSIS  213 

whom  there  is  no  keener  observer,  states  that  he  is  more 
and  more  impressed  with  the  fact  that  overloading  the 
stomach  with  rich  or  heavy  or  spiced  foods  is  today  one  of 
the  first  causes  of  arterial  degeneration.  It  stands  to  rea- 
son that  this  is  true.  We  know  that  organs  exposed  con- 
stantly to  hard  work  undergo  hypertrophy,  and  that  the 
blood  tension  in  those  organs  is  high.  Blood  tension  is, 
after  all,  dependent  on  capillary  resistance,  and  if  the  capil- 
laries are  distended  with  blood,  the  resistance  is  great. 
The  digestive  organs  can  be  no  exception  to  this  rule.  In- 
creased work  means  an  increase  of  blood.  This  inevitably 
causes  distension  of  the  capillaries  with  stretching  of  the 
arteries  and  consequent  damage  to  the  walls.  Once  arterio- 
sclerosis is  present  a  vicious  circle  is  established. 

A  man  about  forty-five  consults  us  and  says  that  he  has 
noticed  recently  that  he  gets  out  of  breath  easily;  in  tying 
his  shoes  he  experiences  some  dizziness.  He  finds  that  he 
has  palpitation  of  the  heart  and  possibly  pain  over  the 
precordial  region  now  and  then.  He  notices  also  that  he  is 
irritable,  that  is,  his  family  tell  him  he  is,  and  he  notices 
that  things  that  formerly  did  not  annoy  him,  now  are  almost 
hateful  to  him.  On  examination,  one  finds  a  palpable  ra- 
dial, a  somewhat  hypertrophied  heart  and  slightly  accen- 
tuated second  aortic  sound.  The  blood  pressure  may  be 
high.  The  urine  may  or  may  not  reveal  any  abnormalities. 
Not  infrequently,  although  no  albumin  may  be  found,  there 
are  hyaline  casts.  Such  a  case  of  arteriosclerosis  is  evi- 
dently not  to  be  regarded  as  early.  Then  the  question 
arises.  How  are  we  to  recognize  early  arteriosclerosis  ?  I 
do  not  believe  that  the  solution  of  this  problem  lies  entirely 
in  the  hands  of  the  physician.  Some  men  are  fortunate 
enough  to  come  up  for  an  examination  for  life  insurance 
before  an  observant  doctor  who  recognizes  the  palpable 
artery,  makes  out  the  beginning  heart  liypertroi)hy  and  the 
slightly  accentuated  second  aortic  sound.  The  patient  will 
tell  you  that  he  never  felt  better  in  his  life.    He  gets  u\)  at 


214  ARTERIOSCLEROSIS 

seven,  works  all  day,  plays  golf,  drinks  liis  three  to  six 
whiskies,  and  is  proud  of  his  physical  development.  But 
the  great  mass  of  people  are  not  fortunate  from  this  stand- 
point. They  do  not  seek  the  advice  of  the  physician  until 
they  are  stretched  out  in  bed.  They  boast  of  the  fact  that 
for  twenty  years  they  have  never  had  a  doctor.  One  may 
well  say  that  it  is  a  problem  how  to  reach  such  persons.  It 
seems  to  me  that  there  can  be  but  one  way  to  do  this.  The 
people  must  be  taught  that  the  duty  of  a  physician  is  just 
as  much  to  keep  them  in  health  as  it  is  to  bring  them  back 
to  health  when  they  are  ill.  To  that  end  people  should  be 
taught  that  at  least  twice  a  year  they  should  be  carefully 
examined.  I  do  not  mean  that  the  patient  should  present 
himself  to  the  doctor  and,  after  a  few  questions  the  doctor 
say  cheerfully,  ''You  are  all  right."  The  patient  should 
be  systematically  examined.  That  means  a  removal  of  the 
clothing  and  examination  on  the  bare  skin.  Such  coopera- 
tion on  the  part  of  patient  and  doctor  would  save  the  pa- 
tient years  of  active  life  and  make  of  the  doctor,  what  his 
position  entitles  him  to  be,  the  benefactor  to  the  community. 
Too  often  careless  work  on  the  physician's  part  lulls  the 
patient  into  a  false  sense  of  security  and  he  wakes  up  too 
late  to  find  that  he  has  wasted  months  or  years  of  life. 
Early  diagnosis  of  arteriosclerosis  is  only  possible  in  excep- 
tional cases  unless  people  present  themselves  to  the  physi- 
cian with  the  thought  in  mind  that  he  is  the  guardian  of 
health  as  well  as  the  healer. 

There  are  patients  who  go  to  the  ophthalmologist  for 
failing  vision.  Physically  they  feel  quite  well.  They  have 
been  heavy  eaters,  hard  workers,  men  and  women  who  have 
been  under  great  mental  strain.  On  examination  of  the 
fundus  of  the  eye  there  is  found  slight  tortuosity  of  the  ves- 
sels with  possibly  areas  of  degeneration  in  the  retina.  A 
careful  physical  examination  will  usually  reveal  the  signs 
of  arteriosclerosis  elsewhere.  We  have  mentioned  fre- 
quently high  tension  as  an  early  sign.    This  must  be  taken 


DIAGNOSIS  215 

with  somewhat  of  a  reservation,  for  this  reason:  not  infre- 
quently a  persistent  high  tension  is  the  earliest  sign  of 
chronic  nephritis.  The  arteries  may  be  pipe  stem  in  char- 
acter and  the  heart  small  and  flabby.  However,  if  one 
watches  for  the  palpably  thickened  superficial  arteries  (al- 
ways bearing  in  mind  the  normal  palpability  as  age  ad- 
vances) and  the  high  tension,  he  can  not  go  far  wrong  in  his 
treatment  whether  the  case  is  one  of  chronic  nephritis  or  of 
arteriosclerosis. 

There  is  also  this  to  bear  in  mind.  Arteriosclerosis  may 
be  marked  in  some  vessels  and  so  slight  in  the  peripheral 
vessels  that  it  can  not  with  certainty  be  made  out.  But 
when  the  radials  are  sclerosed,  it  is  usually  the  case  that 
similar  changes  exist  in  other  parts.  Then  too,  there  may 
be  marked  changes  at  the  root  of  the  aorta  leading  to 
sclerosis  of  the  coronary  vessels  alone,  and  the  first  intima- 
tion that  the  patient  or  any  one  else  has  that  there  is  dis- 
ease, may  be  an  attack  of  angina  pectoris.  Except  for 
symptoms  on  the  part  of  the  heart  there  is  no  way  to  make 
the  diagnosis  of  sclerosis  of  the  coronary  arteries. 

Differential  Diagnosis 

In  arriving  at  a  diagnosis,  when  the  question  is  whether 
or  not  arteriosclerosis  is  the  main  etiologic  factor,  the 
most  important  fact  to  know  is  the  age  of  the  patient. 
Other  points  that  have  been  dwelt  on  fully  must  of  necessity 
also  be  borne  in  mind. 

Possibly  the  chief  conditions  that  may  be  confused  with 
some  of  the  results  of  arteriosclerosis  are  pseudo  angina 
pectoris  which  may  be  mistaken  for  true  angina  pectoris, 
and  ulcer  of  the  stomach,  appendicitis  (?)  or  other  inflam- 
matory abdominal  condition  which  may  be  mistaken  for 
anorina  abdominalis. 

Differential  tables  are  sometimes  of  value  in  fixing  the 
chief  points  of  difference  graphically- 


21G 


MITE  R 1 0.SCLEUOS  I S 


Pseudo  angina  pectoris. 

Etidlogy  ratliiM'  certain;  liystcria, 
ncurastlu'iiia,  toxic  af^oiits,  and  reflex 
irritations. 

Xo  aj^e  is  exenijit.  Usually  in 
youn^    people,    chiefly    females. 

Paroxysms  of  pain  occxir  spontane- 
ously, arc  periodic  and  often  noctur- 
nal. 

Pain,  while  severe,  is  diffuse  and 
sensation  is  of  distension  of  heart. 
No  sense  of  real  anguish. 

Duration  may  be  an  hour  or  more. 

Eestlessncss  and  emotional  symp- 
toms of  causative  conditions  are 
prominent. 

Usually  no  increase  in  arterial  ten- 
sion. 

Prognosis   favorable. 


True    angina    pectoris. 

Etiology  not  certain  but  almost  al- 
ways associated  with  arteriosclerosis 
of  the  coronary  arteries  and  also 
aortic  regurgitation. 

Age  is  important  factor.  Rare  be- 
fore forty,  and  males  usually  affected. 

Paroxysn)s  brought  on  by  overex- 
ertions or  excessive  mental  emotion. 
Rarely  periodic. 

Intense  pain,  radiating  down  arm ; 
heart  felt  as  in  a  vise.  Sense  of  an- 
guish  and   impending   dissolution. 

Duration  from  few  seconds  to  sev- 
eral minutes. 

Silent  and  fixed  attitude,  rigidity 
rather   than    restlessness. 

Arterial  tension  is  as  a  rule  in- 
creased. 

I'rognosis  most  unfavorable. 


Ill    differentiating    between    ulcer   of    the    stomach    and 
angina  abdoniinalis  the  following  points  may  be  of  service: 


Ulcer. 

Occurs  as  a  rule  in  young  persons, 
more   often   females. 

Pain  of  boring  character  increased 
by  food  and  by  certain  positions  with 
food  in  stomach.  Felt  through  to 
left  of  spine. 

Occult    blood. found    in    stools. 

Considerable  anemia  apt  to  be 
present. 

Arterial   tension   usually   low. 


Angina    abdominalis. 

Only  occurs  in  adults  over  forty 
who  have  been  heavy  eaters  and 
drinkers,   mostly   males. 

Pain  cramplike,  diffuse,  although 
more  localized  in  epigastrium.  Not 
necessarily   any  connection  with  food. 

No    occult    l)lood    in    stools. 
Anemia  more  often  absent. 

Arterial  tension  high.  (Splanch- 
nic sclerosis.) 


Diseases  in  Which  Arteriosclerosis  Is  Commonly  Found 

There  are  certain  more  or  less  chronic  diseases  in  which 
arteriosclerosis  is  found  either  as  a  separate  disease  or  as 
a  result  of  the  chronic  disease  itself,  or  the  sclerosis  may  be 
the  cause  of  the  disease.  As  examples  of  the  first  class 
are  diabetes  mellitus  and  cirrhosis  of  the  liver.     As  exam- 


DIAGNOSIS  217 

pies  of  the  second  class  are  chronic  nephritis,  gout,  syphilis, 
and  lead  poisoning.  p]xaniples  of  the  third  class  have  al- 
ready been  fully  descril)ed.  Then  certain  rare  diseases 
that  have  been  briefly  descril^ed  in  this  chapter,  viz.:  Ray- 
naud's disease  and  erythroinelalgia  are  frequently  associ- 
ated with  demonstrable  arteriosclerosis. 


CHAPTER  XI 

PROGNOSIS 

111  a  disease  that  presents  as  many  vagaries  as  arterio- 
sclerosis, it  is  not  possible  to  give  a  certain  prognosis. 
Unfortunately  we  do  not  as  a  rule  see  the  arteriosclerotic 
until  the  disease  is  well  advanced,  or  even  after  some  of  the 
more  serious  complications  have  taken  place.  By  that  time 
the  condition  is  progressive,  and  while  the  prognosis  is 
grave  the  individual  may  live  a  number  of  years. 

It  is  fortunate  for  the  arteriosclerotic  that  mild  grades 
of  the  disease  are  compatible  with  a  fairly  active  life.  The 
disease  in  this  stage  may  become  arrested  and  the  patient 
may  live  many  years.  Not  only  in  the  mild  grades  is  this 
possible.  Even  patients  with  advanced  sclerosis  may  enjoy 
good  health  provided  the  organs  have  not  been  so  damaged 
as  to  render  them  unfit  to  perform  their  functions.  The 
frequency  with  which  we  see  advanced  arteriosclerosis  at 
the  postmortem  table  as  an  accidental  discovery,  attests 
the  truth  of  the  foregoing  statement.  Yet  how  often  does 
it  happen  that  individuals,  apparently  in  the  best  of  health, 
suddenly  succumb  to  an  asthmatic  or  uremic  attack,  an 
apoplexy,  cessation  of  the  heart  beat,  or  a  rupture  of  the 
heart  due  to  arteriosclerosis! 

In  order  to  arrive  at  an  intelligent  opinion  in  regard  to 
prognosis  certain  factors  must  be  taken  into  consideration, 
chief  of  which  are:  the  seat  of  the  sclerosis;  the  probable 
stage;  the  existing  complications;  and,  last  and  most  impor- 
tant, the  patient  himself.  The  whole  man  must  be  studied 
and  even  then  our  prognosis  must  be  most  guarded. 

It  is  much  more  dangerous  for  the  patient  when  the 
process  is  in  the  ascending  portion  of  the  arch  of  the  aorta 
than  when  it  has  attacked  the  peripheral  arteries.  Here, 
at  the  root  of  the  aorta,  are  the  openings  of  the  coronary 

218 


PROGNOSIS  219 

arteries  and  the  arteries  supplying  the  brain  are  close  by. 
The  coronary  arteries  here  control  the  situation.  When 
loud  murmurs  are  heard  at  the  aortic  orifice  and  the  heart 
is  evidently  diseased,  it  is  useful  to  divide  the  endocarditis 
into  two  types,  the  arteriosclerotic  and  the  endocarditic. 
The  etiology  of  the  former  is  sclerosis  and  the  prognosis  is 
grave  because  of  the  liability,  nay  the  probability,  that  the 
orifices  of  the  coronary  arteries  will  become  narrowed. 
The  etiology  of  the  second  type  is  in  most  cases  rheumatic 
fever  or  some  other  infectious  disease,  and  the  prognosis 
is  far  better  than  in  the  first  type.  True,  the  two  may  be 
combined.  In  such  a  case,  the  prognosis  is  entirely  de- 
pendent upon  the  course  of  the  arteriosclerosis. 

The  involvement  of  the  arteries  in  the  kidneys  is  of  con- 
siderable importance,  for  it  is  usually  bilateral  and  wide- 
spread. As  a  rule,  the  disease  makes  but  slow  progress 
jjrovided  that  the  general  condition  of  the  patient  is  good, 
but  at  any  time  from  a  slight  indiscretion  or  for  no  assign- 
able cause,  symptoms  of  renal  insufficiency  may  appear  and 
may  rapidly  prove  fatal. 

It  must  not  be  thought  that  because  the  localization  of 
the  arteriosclerosis  in  the  peripheral  arteries  is  usually  the 
most  favorable  condition  that  it  is  therefore  devoid  of  ill 
effects.  On  the  contrary,  very  serious,  even  fatal,  results 
may  be  brought  about  by  interference  with  the  circulation 
with  resultant  extensive  gangrene  of  the  part  supplied  by 
the  diseased  arteries.  The  amputation  of  a  portion  of  a 
leg,  for  instance,  may  relieve,  to  some  extent,  an  over- 
burdened heart  and  prove  life-saving  to  the  patient,  but  the 
neuritic  pains  are  not  necessarily  relieved.  The  torture 
from  these  pains  mav  be  excruciating. 

No  stage  of  the  disease  is  exempt  from  its  particular 
danger.  In  the  early  stages  of  the  disease  before  the 
artery  or  arteries  have  had  time  to  become  strengthened  by 
proliferation  of  the  connective  tissue,  there  is  the  danger  of 
aneurysm.  Later,  the  very  same  protective  mechanism 
leads  to  stiffening  and  narrowing  of  the  arteries  and  hence 


220  ARTKRIOSCLEIIOSIS 

to  increased  work  on  tlie  inwt  of  the  heart  with  all  of  its 
conse(|uences.  Thronil)()sis  is  favored,  and  where  atherom- 
atous ulcers  are  foi-med,  embolism  is  to  ])e  feared. 

As  the  complications  and  results  of  arteriosclerosis  come 
to  the  front  every  one  must  l)e  considered  by  itself  and  as 
if  it  were  the  true  disease.  There  may  be  a  slight  apojjlec- 
tic  attack  from  which  the  patient  fully  recovers,  but  the 
prognosis  is  now  of  a  grave  character,  as  the  chances  are 
that  another  attack  may  supervene  and  carry  off  the  subject. 
Yet,  after  an  apoplectic  attack,  patients  have  lived  for  many 
years.  Probably  the  most  noted  illustration  of  this  is  the 
life  of  Pasteur.  He  had  at  forty-six  hemiplegia  with  grad- 
ual onset.  He  recovered  with  a  resulting  slight  limp,  did 
some  of  his  l)est  work  after  the  stroke,  and  lived  to  be 
seventy-three  years  old.  Yet  the  exception  but  proves  the 
rule  and  the  prognosis  after  one  apoplectic  stroke  should 
always  be  guarded. 

The  first  attack  of  cardiac  asthma  is  to  be  looked  upon 
as  the  beginning  of  the  end.  The  end  may  be  postponed 
for  some  time,  but  it  comes  nearer  with  every  subsequent 
attack.  One  may  recover  from  what  appears  to  be  a  fatal 
attack  of  cardiac  asthma  accompanied  by  edema  of  the  lungs 
and  irregular,  intermittent,  laboring  heart,  but  the  recov- 
ery is  slow  and  the  chances  that  the  next  attack  will  be  the 
fatal  one  are  increased. 

The  significance  of  all)uminuria  is  difficult  to  determine. 
The  kidneys  secrete  albumin  under  so  many  conditions  that 
the  mere  presence  of  albumin  in  the  urine  may  have  but 
little  prognostic  value.  IVIany  cases  are  seen  where  there  is 
no  demonstrable  albumin,  and  yet  the  patient  may  suddenly 
have  a  cerebral  hemori'hage.  As  a  general  rule  the  urine 
should  be  carefully  examined,  but  not  too  nuich  stress  should 
be  laid  on  the  discovery  of  alliumin  and  casts.  It  is  not 
always  possible  to  determine  the  extent  of  the  kidney  lesion 
by  the  uriiiary  examination,  yet  at  any  time  a  uremic  attack 
may  appeal'  and  prove  fatal. 


PROGXOSIS  221 

After  all  the  most  important  fact  for  the  i)atieiit  is  not 
what  the  pathologist  finds  in  his  kidneys  after  he  is  dead, 
but  what  the  living-  functional  capacity  of  the  kidneys  is. 
This  can  now  be  determined  in  a  variety  of  ways  as  the 
result  of  extensive  work  carried  out  in  quite  recent  years. 
The  simplest  method  of  determining  the  functional  capacity 
of  the  kidneys  is  by  the  injection  into  the  muscles  of  the 
back  of  a  solution  containing  (>  mg.  of  the  drug  phenol- 
sulphonephthalein  in  one  c.c.  of  Huid.  This  comes  already 
prepared  in  ampules,  with  full  directions  for  its  employ- 
ment.* Some  clinicians  use  indigo-carmine  in  place  of 
phthalein.  The  general  consensus  of  ojiinion  is  in  favor 
of  phthalein. 

The  nephritic  test  meal  carefully  worked  out  by  ]\losen- 
tlialt  gives  much  valuable  information.  The  determination 
of  the  nonprotein  nitrogen  or  the  creatinin  in  the  l)lo()d  jdso 
reveals  the  functional  ca])acity  of  the  kidneys. t 

One  might  say  that  the  appearance  of  albumin  in  the 
urine  of  an  arteriosclerotic  where  it  had  not  been  before, 
is  a  bad  sign,  and  in  making  a  prognosis  this  must  be  taken 
into  consideration. 

Bleeding  from  the  nose  is  not  infrecpiently  seen  in  those 
who  have  arteriosclerosis.  It  can  hardly  be  called  a  dan- 
gerous symptom  as  it  can  always  be  controlled  by  tampons. 
There  are  times  when  epistaxis  is  decidedly  beneficial  as  it 
relieves  headache,  dizziness,  and  may  avert  the  danger  of 
a  hemorrhage  into  the  brain  substance.  It  is  rare  to  have 
nose  bleed  except  in  cases  of  high  tension  in  plethoric 
individuals.  ]\Iy  experience  has  been  that  it  has  saved  me 
the  trouble  of  bleeding  the  patient.  It  is  always  of  serious 
import  in  that  it  indicates  a  high  degree  of  tension,  but 
there  is  scarcely  ever  any  innnediate  danger  from  the  nose 
bleed  itself. 

Intestinal  hemorrhage  is  alwavs  a  si'rave  sisn.     As  has 


*I    have    found    the    small    colorimeter    made    by     Hyn^on.     Wcstcolt     and     niinniiif: 
Baltimore,   Mo.,  costing  $5.00,  a  very  practical   instrmnent. 
tMosenthal,  U.  ().  :      Arch.    Int.   Med.,    l')l.S.  xvi,  7^3. 
JMyers  and   I^ough :     Arch.    Int.    Med.,    \<)\S.   .\vi,   S^O. 


222  ARTERIOSCLEROSIS 

been  shown,  arteriosclerosis  of  tlie  splanchnic  vessels  not 
infrequently  occurs,  and  an  eni])olus  or  thrombus  may  com- 
pletely occlude  the  superior  mesenteric  artery.  The 
chances  of  the  establishment  of  a  collateral  circulation  are 
small,  as  the  arteries  of  the  intestines  are  end  arteries. 
Necrosis  of  the  part  follows,  blood  is  found  in  the  stools, 
and  perforation  or  gangrene,  or  both,  are  apt  to  follow. 
There  may  be  blocking  of  small  branches  only,  leading  to 
ulceration  of  the  intestine.  Under  all  conditions  the  prog- 
nosis is  serious. 

The  general  condition  of  the  patient,  his  build,  physical 
strength,  j)owers  of  recuperation,  etc.,  must  be  taken  into 
account  in  giving  a  prognosis.  The  more  powerful  the  in- 
dividual, the  more  favorable,  as  a  rule,  is  the  prognosis,  with 
this  reservation  always  in  mind,  that  the  greater  the  body 
development,  the  greater  is  the  heart  hypertrophy,  and  the 
accidents  from  high  tension  must  not  be  overlooked.  Many 
pun}^  individuals  with  stiff,  calcified  arteries  go  about  with 
more  ease  than  a  robust  man  with  thickened  arteries  only. 
The  differentiation  as  pointed  out  by  AUbutt  (page  186), 
is  well  to  keep  in  mind  in  giving  a  prognosis.  It  can  not  be 
too  strongly  emphasized  that  it  is  the  whole  patient  that  we 
must  consider  and  not  any  one  system  that  at  the  time  hap- 
pens to  be  the  seat  of  greatest  trouble,  and  by  its  group  of 
symptoms  dominates  the  picture. 

It  is  evident  from  what  has  been  said  that  an  accurate 
prognosis  in  arteriosclerosis  is  no  easy  matter.  Were 
arteriosclerosis  a  simple  disease  of  an  acute  character  there 
might  be  grounds  for  giving  a  more  or  less  definite  prog- 
nosis. The  most  that  can  be  said  is  that  arteriosclerosis 
is  always  a  serious  disease  from  the  time  that  symptoms 
begin  to  make  themselves  known.  The  gravity  depends  al- 
together on  the  seat  of  the  greatest  arterial  changes,  and 
is  necessarily  greater  when  the  seat  is  in  the  brain  than 
when  it  is  in  the  legs  or  arms. 

The  attitude  of  the  patient  himself  also  determines  to  a 


PROGNOSIS  223 

great  extent  the  prognosis.  Some  men,  especially  those 
who  have  always  enjoyed  good  health,  turn  a  deaf  ear  to 
warnings  and  instead  of  ordering  their  lives  according  to 
the  advice  of  the  physician,  persist  in  going  their  own  way 
in  the  hope  that  the  luck  that  has  always  been  with  them  will 
continue  to  stand  at  their  elbows.  Neither  firmness  nor 
pleadings  avail  w^itli  some  men.  The  only  salve  for  the  con- 
science of  the  physician  is  that  he  has  done  his  best  to  steer 
the  patient  away  from  the  shoals  and  breakers.  In  others 
who  realize  their  condition  and  take  advantage  of  the  advice 
given  as  to  the  regulation  of  their  lives,  the  prognosis  is 
generally  favorable. 

To  sum  up  the  chapter  in  a  few  words,  I  should  say: 
Always  remember  that  the  jDatient  is  a  human  being;  study 
his  habits  and  character  and  mode  of  life ;  look  at  him  as  a 
whole;  take  everything  into  consideration,  and  give  always 
a  guarded  prognosis. 


CHAPTER  XT! 

PROPHYLAXIS 

Arteriosclerosis  comes  to  almost  every  one  who  lives  out 
his  allotted  time  of  life.  As  has  heen  noted  within,  many 
diseases  and  many  lialnts  of  life  are  conducive  to  the  early 
appearance  of  arterial  degeneration.  Decay  and  degenera- 
tion of  the  tissues  are  necessary  concomitants  of  advanc- 
ing years  and  none  of  us  can  escape  growing  old.  From 
the  period  of  adolescence  certain  of  the  tissues  are  com- 
mencing a  retrograde  metamorphosis,  and  hand  in  hand 
with  this  goes  the  deposit  of  fibrous  tissue  which  later  uiay 
become  calcified.  The  arterial  tissue  is  no  exception  to  this 
7'ule,  and  we  have  already  shown  that  certain  changes  nor- 
mally take  place  as  the  individual  grows  older,  changes 
which  are  arteriosclerotic  in  type  and  are  quite  like  those 
caused  in  younger  people  by  many  of  the  etiologic  factors 
of  the  disease. 

We  are  absolutely  dependent  upon  the  integrity  of  our 
hearts  and  blood  vessels  for  the  maintenance  of  activity  and 
span  of  life.  Respiration  may  cease  and  l)e  carried  on  arti- 
ficially for  many  hours  Avliih^  tlie  heart  continues  to  beat. 
Kveii  the  heart  has  ])een  massaged  and  the  individual  has 
been  brought  back  to  life  after  its  i:)ulsations  have  ceased, 
but  such  cases  are  few  in  number.  AVe  can  not  live  without 
the  heart  ])eat  and  the  prophylaxis  of  arteriosclerosis  con- 
sists in  the  adjustment  of  our  lives  to  our  environment,  so 
that  we  may  get  tlie  maxinmm  amount  of  Avork  accomj)lished 
with  the  minimum  amount  of  weai*  and  tear  on  the  blood 
vessels. 

The  struggle  foi-  existence  is  keen.  Competition  in  every 
profession  or  trade  is  exceedingly  acute,  so  nmch  so  that  to 
rise  to  the  head  in  any  l)ranch  of  human  activity  requires 


PROPITYIAXIS  225 

exceptional  powers  of  iiiincl.  Amoii^  those  who  are  entered 
in  this  keen  competition,  the  fittest  only  can  survive  for  any 
period  of  time.  Tlie  weaklings  are  bound  to  succumb.  A 
scion  of  healthy  stock  will  stand  the  wear  and  tear  far  better 
than  will  the  progeny  of  diseased  parentage. 

It  is  only  necessary  to  call  attention  to  the  part  that 
alcohol,  syphilis  and  insanity  play  in  heredity.  These  have 
been  discussed  fully  in  the  earlier  part  of  this  book. 

We  live  rapidly,  burning  the  candle  at  both  ends.  It  is 
not  strange  that  so  many  comparatively  young  men  and 
women  grow  old  prematurely.  AVhile  heredity  is  a  factor 
as  far  as  the  prophylaxis  of  arteriosclerosis  is  concerned, 
of  far  more  importance  is  the  mode  of  life  of  the  individ- 
ual. Scarcely  any  of  us  lead  strictly  temperate  lives.  If 
we  do  not  abuse  our  bodies  by  excessive  eating  and  drink- 
ing and  so  wear  out  our  splanchi.iic  vessels  and  cause  gen- 
eral sclerosis  by  the  high  tension  thereby  induced,  we  abuse 
our  bodies  by  excessive  brain  work  and  worry  with  all  their 
multitudinous  evils.  The  prophylaxis  of  arteriosclerosis 
might  well  be  labeled,  "The  plea  for  a  more  rational  mode 
of  life."  Moderation  in  all  things  is  the  keynote  to  health, 
and  to  grow  old  gracefully  is  an  art  that  admits  of  cultiva- 
tion. Excesses  of  any  kind,  be  they  mental,  moral,  or 
physical,  tend  to  wear  out  the  organism. 

People  habitually  eat  too  much;  many  drink  too  much. 
They  throw  into  the  vascular  system  excessive  fluid  com- 
bined frequently  with  toxic  products  that  cause  eventually 
a  condition  of  high  arterial  tension.  It  has  been  shown  how 
poisonous  substances  absorbed  from  the  intestines  have 
some  influence  on  the  blood  pressure.  Anything  that  causes 
constant  increase  of  pressure  should  be  studiously  avoided. 

Mild  exercise  is  an  essential  feature  of  prophylaxis.  One 
may,  by  judicious  exercise  and  diet,  make  of  himself  a 
powerful  muscular  man  without,  at  the  same  time,  raising 
his  average  blood  pressure.  The  man  who  goes  to  excess 
and  continually  overburdens  his  heart,  will  suffer  tlie  con- 


226  ARTERIOSCLEIlOSrS 

so(iU('iiees,  for  the  l)ill  witli  ('Oinpouiid  interest  will  he 
('liai-.i>('(l  against  him.  It  is  a  great  mistake  for  any  one  to 
work  incessantly  with  no  physical  relaxation  of  any  kind, 
and  yet,  after  all,  it  is  not  so  nuieli  physical  relaxation  that 
is  necessary,  as  the  pnrsnit  of  something  entirely  different, 
so  that  the  mind  may  be  carried  into  channels  other  than 
the  accnstomed  routes.  Diversification  of  interests  is  as  a 
rule  restful.  That  is  what  every  man  who  reaches  adult 
life  should  aim  at.  Hobbies  are  sometimes  the  salvation  of 
men.  They  may  be  ridden  hard,  but  even  then  they  are 
helpful  in  bearing  one  completely  away  from  daily  cares 
and  worries.  The  man  who  can  keep  the  balance  between 
his  mental  and  physical  work  is  the  man  Avho  will,  other 
things  being  equal,  live  the  longest  and  enjoy  the  best 
health. 

Nowadays  the  trend  of  medicine  is  toward  prophylaxis. 
AVe  give  the  state  authority  to  control  epidemics  so  far  as 
it  is  possible  by  modern  measures  to  control  them. 

We  urge  over  and  over  again  the  value  of  early  diagnosis 
in  all  chronic  diseases,  for  we  know  that  many  of  them,  and 
this  applies  particularly  to  arteriosclerosis,  could  be  pre- 
vented from  advancing  by  the  recognition  of  the  condition 
and  the  institution  of  proper  hygienic  and  medicinal  treat- 
ment. 

It  is  the  patent  dufij  of  every  physician  to  instruct  the 
members  of  his  clientele  in  the  fundamental  rides  of  health. 
Recently  the  President  of  the  American  Medical  Associa- 
tion, in  his  address  l)efore  the  1908  meeting,  urged  the 
dissemination  of  accurate  knowledge  concerning  diseases 
among  the  laity.  AVhile  this  may  l)e  done  by  city  and  state 
boards  of  health,  it  seems  far  better  for  the  inodern  trained 
physician  to  work  among  his  own  people.  AVith  concise 
information  concerning  the  modes  of  infection  and  the  dan- 
gers of  waiting  until  a  disease  has  a  firm  hold  ])efore  con- 
sulting the  health  mender,  people  should  be  al)le  to  protect 
themselves  from  infections  and  be  al)le  to  nip  chronic  proc- 


PROPHYLAXIS  227 

osscs  ill  llie  l)iul.  I>ut  it  is  difficult  to  turn  tlie  avci'a.no 
individual  away  IVoiii  tlic  liabit  of  having'  a  dru.g-ck'rk  i)ro- 
scribe  a  dose  of  iiicdieino  for  the  ailment  that  troubles  him. 
It  is  really  unfortunate  that  most  of  the  pains  and  aehes  and 
morbid  sensations  that  one  has  speedily  pass  away  with 
little  or  no  treatment.  Herein  lies  the  stren<;th  of  charla- 
tanism and  quackery.  Unfortunate,  yes,  for  a  man  can  not 
tell  whether  the  trivial  complaint  from  which  he  suffers  is 
any  different  from  the  one  that  was  so  easily  coiKpiered  six 
months  ag'o.  But  instead  of  recovering-,  he  grows  worse. 
JTope  that  springs  eternal  in  the  human  breast,  leads  him 
to  dilly-dally  until  he  at  last  seeks  medical  advice,  only  to 
find  that  the  disease  has  made  such  progress  that  little  can 
be  done. 

In^trU'Ct  the  public  to  consult  the  doctors  twice  a  year. 
The  dentists  have  their  patients  return  to  them  at  stated 
intervals  only  to  see  if  all  is  well.  Iloir  much  more  rational 
it  ivould  he  if  men  and  jromen  past  the  age  of  forty  had 
a  physical  examination  made  twice  a  year  to  find  out  if  all 
is  IV ell. 

The  prophylaxis  of  arteriosclerosis  is  moderation  in  all 
the  duties  and  ])leasures  of  life.  This  in  no  sense  means 
that  a  man  has  to  nurse  himself  into  neurasthenia  for  fear 
that  something  will  happen  to  him.  As  one  grows  in  years 
exercise  should  not  be  as  violent  as  it  was  when  younger, 
and  food  should  lie  taken  in  smaller  ([uantities.  ^taiiy  forms 
of  exercise  suggest  themselves,  particularly  walking  and 
golf.  Walking  is  a  much  neglected  form  of  exercise  which, 
in  these  modern  days  with  our  thousand  and  one  means  of 
locomotion,  is  becoming  almost  extinct.  There  is  no  better 
form  of  exercise  than  graded  walking.  To  strengthen  the 
heart  selected  hill  climliing  is  one  of  the  best  therajieutic 
methods  that  we  have.  The  patient  is  made  to  exercise  his 
heart  just  as  he  is  made  to  exercise  his  legs,  and  as  with 
exercise  of  voluntary  muscles  conies  increase  in  strength, 
so  by  fitting  exercise  may  the  heart  muscle  be  incr(vised  in 


228  AETERTOSCLEROSIS 

power.  A  warning  sliould  be  sounded,  however,  against 
over  exercise.  This  leads  naturally  to  hypertrophy  Avith 
all  its  disastrous  possibilities.  Men  who  have  been  athletes 
when  young  should  guard  against  overeating  and  lack  of 
exercise  as  they  grow  older.  Many  of  the  factors  which 
favor  the  development  of  arteriosclerosis  are  already  there, 
and  a  sedentary,  ordinary  life,  such  as  office  all  day,  club 
in  afternoon,  a  few  drinks  and  much  rich  food,  will  inevi- 
tably lead  to  well-advanced  arterial  disease. 

Karl  Marx  in  his  famous  Socialistic  platform  said:  ''No 
rights  without  duties;  no  duties  without  rights."  So  we 
may  paraphrase  this  and  say:  "No  brain  work  without 
moderate  physical  exercise  in  the  open  air;  no  physical  ex- 
ercise without  moderate  brain  work. ' ' 

There  is  yet  one  other  point  that  is  important,  the  com- 
bination of  concentrated  brain  work  and  constant  whiskey 
drinking.  This  is  most  often  seen  in  men  of  forty-five  to 
fifty-five,  heads  of  large  business  concerns  who  habitually 
take  from  six  to  twelve  drinks  of  whiskey  daily,  and  with 
possibly  a  bottle  of  wine  for  dinner.  Such  men  appear 
ruddy  and  in  prime  health  but,  almost  invariably,  careful 
examination  will  reveal  unmistakable  signs  of  arterial  dis- 
ease. There  is  usually  the  enlarged  heart  and  pulse  of  high 
tension  with  or  without  the  trace  of  albumin  in  the  urine. 
The  lurking  danger  of  this  group  of  manifestations  has  so 
impressed  the  medical  directors  of  several  of  the  large  in- 
surance companies  that  a  blood  pressure  reading  must  be 
made  on  all  applicants  over  forty  years  of  age.  Should  high 
blood  pressure  be  found,  the  premium  is  increased,  as  the 
expectation  of  life  is  proportionately  shorter  in  such  men 
than  in  normal  persons. 

Therefore,  let  every  physician  act  his  part  as  guardian 
of  health.  Only  in  this  way  is  the  prophylaxis  of  arterio- 
sclerosis possible. 


CHAPTER  XIII 


TREATMENT 


Although  it  has  been  rather  dogmatically  stated  (vide 
supra)  that  every  one  who  reaches  old  age  has  arterioscle- 
rosis, it  must  not  l)e  inferred  that  absolutely  no  excejotions  to 
this  rule  are  found.  Cases  are  known  where  persons  of 
ninety  years  even  had  soft  arteries,  and  we  have  seen  per- 
sons of  eighty  whose  arteries  could  not  be  palpated.  When 
infants  and  children  are  seen  with  considerable  sclerosis, 
it  proves  that,  after  all,  it  is  the  quality  of  the  tissue  even 
more  than  the  wear  and  tear,  that  is  the  determining  factor 
in  the  production  of  arteriosclerosis.  It  would  be  Avell  if 
those  who  can  not  bring  healthy  progeny  into  the  Avorld 
were  to  leave  this  duty  to  those  who  can. 

In  general  the  treatment  of  arteriosclerosis  is  prophylac- 
tic and  symptomatic.  In  the  preceding  chapter  I  had  some- 
thing to  say  about  prophylaxis  in  general;  I  must  again 
refer  to  it  in  detail. 

Arteriosclerosis  is  essentially  a  chronic  progressive  dis- 
ease, and  the  secret  of  success  in  the  management  of  it  is 
not  to  treat  the  disease  or  the  stage  of  the  disease,  but  to 
treat  the  patient  who  has  the  disease.  To  infer  the  stage 
of  the  disease  from  the  feeling  of  the  sclerosed  artery,  may 
lead  to  serious  mistakes.  Persons  with  calcified  arteries 
may  be  perfectly  comfortable,  while  those  with  only  moder- 
ate thickening  may  have  many  severe  symptoms.  The 
keynote  is  individualization.  It  is  manifestly  absurd  to 
treat  the  laboring  man  witli  his  arteriosclerosis  as  one 
would  treat  the  successful  financier.  The  habits,  mode  of 
life,  every  detail,  should  be  studied  in  every  patient  if  we 
expect  to  gain  the  greatest  measure  of  success  in  the  treat- 
ment.   One  may  treat  fifty  patients  who  have  typhoid  fever 

229 


230  Ai;TKiti(>sc'J.Ki;()sis 

l)y  a  I'outine  iiiethod  and  all  may  recover.  Individualizing", 
while  of  ^-reat  value  in  the  treatment  oi'  aeute  diseases,  yet 
is  not  absolutely  essential  in  order  that  good  results  may 
be  obtained.  Far  different  is  it  when  treatin<^'  a  disease 
like  arteriosclerosis.  One  wlio  relies  on  textl)()ok  knowl- 
ed.ge  Avill  find  liimselt*  at  a  loss  to  know  what  to  do.  Text- 
])0()ks  can  only  outline,  in  the  briefest  manner,  the  average 
case,  and  no  one  ever  sees  the  average  book  case.  At  the 
bedside  with  the  patients  is  the  place  to  learn  therapeutics 
as  well  as  diagnosis.  All  that  can  be  hoped  for  in  outlining 
the  ti'eatment  of  arteriosclerosis  is  to  lay  doMii  a  few  prin- 
ci])les.  The  tact,  the  intuition,  the  sul)tle  something  that 
makes  the  successful  therapeutist,  can  not  be  learned  from 
books.  80  the  man  who  treats  cases  l)y  rule  of  tliuml)  is  a 
failure  from  the  beginning.  There  are  certain  general 
principles  that  will  be  our  sheet  anchors  at  all  times  and 
for  all  cases.  The  art  of  varying  the  application  of  these 
fundamentals  to  suit  the  individual  case,  is  not  to  be  culled 
from  printed  words. 

Hygienic  Treatment 

Every  man  is  more  or  less  the  arbiter  of  his  own  fate. 
Granted  that  he  has  good  tissue  to  begin  life,  his  own  habits 
and  actions  determine  his  span  of  comfortable  existence. 
No  one  cares  to  live  after  his  brain  begins  to  fail,  and  the 
failing  brain  is  often  due  to  disease  of  the  cranial  arteries. 
The  hygienic  treatment  resolves  itself  into  advice  in  regard 
to  prophylaxis. 

First  and  foremost  is  exercise.  It  has  seemed  to  ns  that 
the  revival  of  out-of-door  sports  is  one  of  the  best  signs  of 
promise  of  the  i)reservation  of  a  virile,  hardy  race.  That 
women,  as  well  as  men,  indulge  in  the  lighter  forms  of  out- 
of-door  exercise  should  ])ring  it  about  that  the  coming 
generation  will  start  in  life  under  the  most  advantageous 
conditions  of  bodily  resistance. 

Among  all  the  forms  of  exercise,  golf  probably  is  the  best. 


TIIEATMEXT  231 

It  is  not  too  violent  for  the  middle-aged  man,  yet  it  gives 
the  young  athlete  quite  enough  exercise  to  tire  him.  It  is 
plajx'd  in  the  open.  One  is  compelled  to  walk  up  and  down 
in  pleasant  company,  for  golf  is  essentially  a  conipaniona])le 
game,  while  he  reaps  the  full  benefit  of  the  invigorating  ex- 
ercise. The  blood  courses  tli  rough  the  nmscles  and  lungs 
more  rapidly;  the  contraction  of  the  skeletal  muscles  serves 
to  compress  the  veins  and  so  to  aid  the  return  of  blood  to 
the  heart:  the  lungs  are  rendered  hyperemic,  deeper  and 
fuller  breaths  must  be  taken;  oxidation  is  necessarily  more 
rapid,  and  effete  pi'oducts,  whicli  if  not  completely  oxidized 
Avould  possibly  act  as  vasoconstrictors,  are  oxidized  to 
harmless  products  and  eliminated  witliout  irritating  the 
excretory  organs. 

Other  forms  of  out-door  exercise  that  can  be  recom- 
mended are  tennis,  canoeing,  rowing,  fishing,  horseback  rid- 
ing, swimming,  etc.  Tennis  is  the  most  violent  of  all  the 
sports  mentioned  and  might  readily  be  overdone.  Rowing 
as  practiced  by  the  eights  at  college  is  undoubtedly  too  vio- 
lent a  form  of  exercise,  and  may  be  productive  in  later  life 
of  very  grave  results.  Canoeing  is  a  delightful  and  in- 
vigorating exercise.  The  muscles  of  the  arms,  shoulders, 
and  trunk  are  especially  used,  the  leg  nuiscles  scarcely  at 
all.  Nevertheless,  the  deep  breathing  that  necessarily 
comes  with  all  chest  exercises  aerates  every  portion  of  the 
lungs,  and  is  of  great  benefit  to  tlie  whole  body. 

Swinmiing  as  an  exercise  lias  nuich  to  reconnneiid  it.  In 
this  sport  all  the  nmscles  take  jiart  and  at  the  same  time  the 
chest  is  broadened  and  dee})ened. 

All  these  methods  of  using  the  nuiscles  to  keep  oneself  in 
trim,  so  to  speak,  are  part  and  parcel  of  the  general  hygienic 
mode  of  life  that  is  conducive  to  a  healthy  old  age.  Exer- 
cise can  be  overdone,  as  eating  can  be  overdone.  Both  are 
essential  and  yet  both  can  ])e  the  means  of  hastening  an  in- 
dividual to  a  premature  grave. 

When  the  arteriosclerosis  has  advanced  so  far  that  it  is 


232  ARTERIOSCLEROSIS 

easily  recognizable,  certain  forms  of  exercise  should  be  abso- 
lutely prohibited.  Such  are  tennis,  rowing  and  swimming. 
Horseback  riding  to  be  allowed  must  be  strictly  supervised. 
At  times  this  may  be  an  exceedingly  violent  exercise.  As 
an  out-of-door  sport,  there  is  nothing  that  equals  golf. 
The  physician,  knowing  the  character  of  the  course,  and 
the  length  of  it,  can  say  to  his  patient  that  he  may  play  six, 
nine,  twelve,  or  eighteen  holes,  depending  on  the  patient's 
condition. 

For  those  who  are  not  able  to  get  out,  exercise  in  the 
room  with  the  windows  open  must  take  the  place  of  out-of- 
door  sports.  Here  the  use  of  chest  weights  is  a  most 
excellent  means  of  keeping  up  the  tone  of  the  muscles.  By 
adjusting  the  weights,  the  exercise  may  be  made  light, 
medium,  or  heavy.  Every  physician  should  bo  familiar 
with  the  chest  weight  exercises.  They  are  not  as  good  as 
open  air  exercise  but  they  undoubtedly  have  been  the  means 
of  saving  3^ears  of  life  to  many  patients  with  arterial 
disease. 

There  comes  a  time  when  all  forms  of  exercise  must  be 
prohibited  on  account  of  the  dyspnea,  edema,  dizziness,  etc. 
It  seems  unwise  to  keep  such  a  patient  in  bed,  even  though 
the  edema  be  considerable.  Once  on  his  back  in  bed  he 
becomes  weak,  and  the  danger  of  edema  of  the  lungs  or 
hypostatic  congestion  of  the  bases,  with  subsequent  bron- 
chopneumonia, is  very  great. 

Such  patients  may  be  allowed  to  sit  up  in  a  comfortable 
chair  with  the  legs  supported  straight  out  on  a  stool  or 
other  chair.  The  half  reclining  position  is  not  easy  to  as- 
sume in  bed.  Considerable  ingenuity  must  often  be  exer- 
cised by  the  physician  in  making  the  patient  comfortable 
without  increasing  the  symptoms  from  which  the  patient 
suffers  following  the  least  amount  of  exercise.  Although 
such  persons  can  not  exercise  actively,  they  should  have 
passive  exercise  in  the  form  of  massage,  carefully  given,  so 
that  no  injury  is  done  to  the  rigid  vessels.    It  is  possible  to 


TREATMENT  233 

rupture  a  vessel,  tlie  walls  of  which  are  encrusted  with  lime 
salts,  and  full  of  small  aneurysmal  dilatations.  Every  pa- 
tient must  be  watched  carefully  and  measures  instituted  for 
the  individual. 

Balneotherapy 

As  a  tonic  and  invigorator,  the  cold  or  cool  bath  (shower 
or  tub),  in  the  morning  on  arising  can  be  highly  recom- 
mended. It  promotes  skin  activity,  is  a  stimulant  to  the 
bowels  and  kidneys  and  to  the  general  circulation,  besides 
being  cleansing.  We  find  today  that  the  morning  bath  has 
become  such  a  necessity  to  the  average  American  that  all 
new  hotels  are  fitted  with  private  baths,  and  old  hotels,  iu 
order  to  get  patronage,  are  arranging  as  many  baths  con- 
nected with  sleeping  rooms  as  is  possible.  Our  generation 
assuredly  is  a  ruddy,  clean-bodied  one.  What  the  actual 
results  of  this  out-door  life  and  frequent  bathing  will  be 
for  the  race  remains  to  be  seen,  but  one  can  not  but  feel 
that  it  must  build  up  a  stronger,  more  resistant  race  of 
people,  who  not  only  enjoy  better  health  than  did  their  fore- 
fathers, but  enjoy  it  longer. 

Not  every  one  can  stand  a  cold  bath.  It  is  folly  to  urge 
it  on  one  to  whom  it  is  distasteful,  or  on  one  who  does  not 
feel  the  comfortable  glow  that  should  naturally  result.  For 
the  well,  or  those  with  a  tendency  to  arteriosclerosis,  or 
those  in  whose  families  there  have  been  several  members 
who  had  early  arteriosclerosis,  such  proceedings  as  recom- 
mended could  not  be  improved  upon.  How^ever,  for  the 
person  who  has  well  recognized  sclerosis,  only  warm  baths 
should  be  advised,  and  these  not  daily.  The  water  should 
be  at  a  temperature  of  90-95°  F.  Care  should  be  taken 
that  persons  sent  to  spas  be  cautioned  against  hot  baths. 
It  is  not  inconceivable  that  the  increased  force  of  the  heart 
beat  that  accompanies  a  hot  bath  might  be  sufficient  to  rup- 
ture a  small  cranial  vessel.  Hence,  Turkish  and  Russian 
baths  should  be  most  unqualifiedly  condemned.    As  a  mat- 


234  AHTEIUOSCLEHOSIS 

ter  of  fact,  persons  vary  so  in  their  liabits  with  regard  to 
bathing  that  what  might  suit  one  person  would  do  another 
much  harm. 

Personal  Habits 

The  personal  habits  of  the  individual,  more  than  any 
other  factor,  determine  whether  or  not  arteriosclerosis  sets 
in  early  in  his  life.  The  man  or  woman  who  is  moderate  in 
eating  and  drinking,  sees  that  the  kidneys  are  kept  in  good 
condition,  and  attends  strictly  to  regularity  of  the  bowels, 
lays  a  good  basis  for  the  measure  of  health  which  is  so 
essential  for  happiness.  It  has  been  shown  that  sclerosis 
of  the  splanchnic  vessels  may  be  due  to  constant  irritation 
of  toxic  products  elaborated  in  digesting  constantly  enor- 
mous meals.  In  obstinate  constijDation,  many  poisons,  the 
nature  of  which  we  do  not  know,  are  absorbed  and  circulate 
in  the  blood.  We  have  not  sufficient  data  to  prove  that 
constipation  favors  the  production  of  arteriosclerosis,  but 
our  impression  has  been  that  it  does  favor  it.  Constipa- 
tion can  often  be  relieved  by  a  glass  of  water  before  break- 
fast, a  regular  time  to  go  to  stool,  and  abdominal  massage 
or  exercises.  Some  maintain  that  it  is  a  bad  habit  only, 
and  can  be  readily  overcome.  Whatever  is  done,  avoid 
leading  the  patient  into  the  drug  habit,  for  the  last  state 
of  the  patient  will  be  worse  than  the  first.  Habits  of  sleep 
are  not  of  such  great  importance.  Most  persons  get  enough 
sleep  except  when  under  severe  mental  strain.  Most  adults 
need  from  seven  to  eight  hours'  sleep,  although  some  can 
do  all  their  work  and  keep  in  prime  health  on  five  or  six 
hours'  sleep. 

Tobacco  has  been  accused  of  causing  many  ills  and  has 
been  thereby  much  maligned.  We  can  not  see  that  the  use 
of  tobacco  in  any  form  in  moderation  is  harmful  to  most 
men.  Undoulitedly  the  blood  pressure  is  raised  when  mild 
tol)aeco  poisoning  occurs,  and  individual  peculiarities  of  re- 
action to  the  weed  are  multitudinous.    But  to  condemn  off- 


TItEATMENT  235 

hand  its  use  is  the  height  of  folly.  There  is  no  reason  why 
the  arteriosclerotic  who  has  always  used  tol)acco  in  modera- 
tion, sliould  not  continue  to  use  it,  whetlier  he  smoke  ciga- 
rettes, cigars,  or  pipe.  His  supply  should  be  decreased,  but 
there  is  no  sense  in  depriving  a  man  of  one  of  the  solaces  of 
life,  unless,  as  is  sometimes  the  case,  a])stinence  is  easier 
for  the  patient  than  moderation. 

As  for  ak'ohol,  o])inions  differ  widely.*  Some  see  in  al- 
cohol one  of  the  most  frequent  causes  of  arteriosclerosis; 
others  do  not  believe  that  the  part  played  by  alcohol  is  a 
serious  one,  only  in  conjunction  with  other  poisonous  sub- 
stances is  it  dangerous.  Probably  unreasoning  fanaticism 
has  had  much  to  do  with  the  wholesale  condemnation  of 
alcoholic  beverages.  The  general  effect  of  alcohol  is  to 
lower  the  blood  pressure  by  causing  marked  dilatation  of 
all  the  vessels  of  the  skin.  True,  the  alcohol  circulates  in 
the  blood,  and  is  broken  up  in  the  liver,  and  this  organ 
would  seem  to  bear  the  brunt  of  the  harm  done.  Alcoholic 
drinks  in  moderation,  I  do  not  believe  have  any  deleterious 
effect  on  health.  On  the  contrary,  I  believe  that  they  may 
in  some  cases  assist  digestion  and  assimilation.  Indiscrim- 
inate indulgence  is  to  be  condemned,  as  is  overindulgence 
in  exercise  or  eating.  AVhat  may  be  moderate  for  A,  might 
be  excessive  for  B.  Every  man  is  then  the  arbiter  of  his 
own  fortune  and  within  his  own  limits  can  indulge  moder- 
ately (a  relative  term  after  all)  without  fear  of  doing  him- 
self harm.  In  advanced  arteriosclerosis  it  is  necessary  to 
decrease  the  sui)ply  of  alcohol  just  as  it  is  necessary  to  cut 
down  the  food  supply.  This  must  rest  entirely  on  the 
judgment  of  the  ])hysician,  who  must  not  act  arbitrarily, 
but  nmst  have  his  reasons  for  every  one  of  his  orders. 

Dietetic  Treatment 

Most  persons  eat  too  much.  We  not  oidy  satisfy  our 
hunger,  but  we  satisfy  our  palates,  and,  instead  of  putting 

•Discussion  of  alcohol  at  i)rcsent  has  value  ouly  as  it  relates  to  tlie  jiast.  The  iiicscnt 
is  dry.      The   future   is  in   the   laji  of  the   gods. 


236  ARTERIOSCLEROSIS 

substantial  foodstuffs  into  our  stomachs,  we  frequently  take 
unto  ourselves  concoctions  that  defy  description. 

Foodstuffs  are  composed  of  one  or  all  of  three  classes: 
(1)  proteins,  (2)  fats,  (3)  carbohydrates.  As  examples 
of  the  first  are  beef  and  white  of  egg;  of  the  second,  the 
oils,  butter,  lard ;  of  the  third,  sugar,  potato,  beet,  corn,  etc. 

The  physiologists  and  chemists  have  shown  us  that  both 
endogenous  and  exogenous  uric  acid  in  excess  will  cause  a 
rise  of  blood  pressure,  but  the  bodies  most  concerned  in 
the  production  of  elevated  blood  pressure  are  the  purin 
bodies,  those  organic  compounds  which  are  formed  from 
proteins  and  represent  chemically  a  step  in  the  oxidation 
of  part  of  the  protein  molecule  to  uric  acid.  Red  meat 
contains  more  of  the  substances  producing  purin  bodies 
than  any  other  one  common  foodstuff,  and  for  this  reason 
the  excessive  meat  eater  is,  ceteris  paribus,  more  apt  to 
develop  arteriosclerosis  comparatively  early  in  life. 

The  fats  and  carbohydrates  contain  practically  no  sub- 
stances that  react  on  the  body  of  the  ordinary  individual 
in  a  deleterious  manner  during  their  digestion.  The  extra 
work  that  is  put  on  the  heart  by  the  formation  of  many 
new  blood  vessels  in  adipose  tissue  is  the  only  harmful  effect 
of  overindulgence  in  these  foodstuffs. 

It  has  been  found  that  nitrogen  equilibrium  can  be  main- 
tained at  a  wide  range  of  levels.  Formerly  135-150  gms. 
of  protein  daily  were  considered  necessary  for  a  man  doing 
light  work.  Now  it  is  known  that  half  that  amount  is  suf- 
ficient to  keep  one  in  nitrogenous  equilibrium,  and  to  enable 
one  to  keep  his  weight.  A  person  at  rest  requires  even  less 
than  that.  One  who  is  engaged  in  hard  physical  labor  burns 
up  more  fuel  in  the  muscles,  and  so  must  have  a  larger 
fuel  supply. 

Although  we  habitually  eat  too  much  we  drink  too  little 
water.  For  those  who  have  any  form  of  arterial  disease 
an  excess  of  fluid  is  harmful,  as  the  vessels  become  filled 
up  and  a  condition  of  plethora  results,  which  necessarily 


TREATMENT  237 

reacts  injuriously  on  the  heart  and  circulation.  The  drink- 
ing? of  a  glass  of  water  during  meals  is,  in  the  author's 
opinion,  good  practice.  The  water  must  be  taken  mouthful 
at  a  time,  and  not  gulped  down.  If  this  is  done,  there 
results  sufficient  dilution  of  the  solid  food  to  enable  the 
gastric  juices  successfully  and  rapidly  to  reach  all  parts 
of  the  meal. 

Some  are  in  favor  of  a  rigid  milk  diet  for  those  who 
have  arteriosclerosis.  Some  men  have  lived  on  nothing 
but  milk  for  several  years  and  have  not  only  kept  in  good 
health,  but  have  actually  gained  weight  and  led  at  the 
same  time  active  lives.  It  has  been  held  by  others  that  rigid 
milk  diet  is  positively  harmful  on  account  of  the  relatively 
large  quantity  of  calcium  salts  that  are  ingested.  This  was 
thought  to  favor  the  deposition  of  calcareous  material  in 
the  walls  of  the  already  diseased  arteries.  While  possibly 
there  may  be  some  danger  of  increased  calcification,  the 
majority  of  clinicians  are  in  favor  of  a  milk  cure  given  at 
intervals.  Thus  the  patient  is  made  to  take  three  to 
four  quarts  daily  for  a  period  of  a  month.  There  is  then  a 
gradual  return  to  a  general  diet,  exclusive  of  meat,  for 
several  weeks,  then  another  rigid  milk  diet  period. 

If  we  are  bold  enough  to  follow  Metschnikoff  in  his  tlieo- 
ories  of  longevity,  we  might  advise  resection  of  the  large 
intestine,  on  the  ground  that  it  is  an  enormous  culture  tube 
that  produces  prodigious  amounts  of  i^oisonous  substances 
which  are  thrown  into  the  general  circulation.  To  combat 
such  a  grave  (?)  condition  as  the  carrying  of  several  feet 
of  large  intestine,  we  are  recommended  to  take  buttermilk 
or  milk  soured  by  means  of  the  h.  aciclus  lacticus.  Clinical 
experience  has  taught  that  in  arteriosclerosis  buttermilk 
is  of  great  value,  whether  it  be  the  natural  product,  or  made 
directly  from  sweet  milk  by  the  addition  of  the  bacilli.  The 
latter  is  a  smoother  product  and  has,  to  my  mind,  a  de- 
lightful flavor.  It  may  be  diluted  with  Vichy  or  plain  soda 
water.    Cases  that  can  not  take  milk  or  anv  other  food  will 


238  ARTERIOSCLEROSIS 

often  take  ])iittenHilk,  and  do  well  on  this  restricted  diet. 
From  two  to  four  quarts  daily  should  be  taken.  It  should 
be  drunk  slowly  as  should  milk. 

Medicinal 

It  has  long  been  thought  that  the  iodides  have  some  spe- 
cific effect  on  the  advancing  arteriosclerosis,  checking  its 
spread,  if  not  really  aiding  nature  to  a  limited  restoration 
of  the  diseased  arteries.  It  is  possible  that  the  eulogies 
upon  the  iodides  owe  their  origin  to  the  successful  treat- 
ment of  syphilitic  arteriosclerosis,  in  which  condition  these 
drugs  have  a  specific  action.  However  that  may  be,  there 
is  no  doubt  that  the  administration  of  sodium  or  potassium 
iodide  is  good  therapeutics  in  cases  of  arteriosclerosis. 

Unfortunately  many  persons  have  such  irritable  stom- 
achs that  they  can  not  take  the  iodides,  even  though  they  be 
diluted  many  times.  They  may  be  made  less  irritating  by 
giving  them  with  essence  of  jjepsin.  Unless  the  case  is 
syphilitic,  it  is  doubtful  whether  it  is  of  value  to  increase  the 
dose  gradually  until  a  dram  or  even  more  is  taken  three 
times  daily  after  meals.  Usually  a  maximum  dose  of  ten 
grains  seems  to  be  quite  sufficient.  This  may  be  taken  three 
times  a  day,  well  diluted,  for  three  months.  There  follows 
a  month's  rest,  then  the  treatment  is  resumed  for  another 
period  of  three  months,  and  so  on.  Either  sodium  or  potas- 
sium iodide  in  saturated  solution  may  be  given.  The  so- 
dium salt  is  possibly  less  irritating,  and  contains  more  free 
iodine  than  the  potassium  salt,  although  the  latter  is  more 
generally  used.    The  strontium  iodide  may  also  be  used. 

One  sees  a  patient  now  and  then  who  can  not  take  the 
iodides,  however  they  may  be  combined.  For  such  patients 
one  may  obtain  good  results  with  iodopin,  sajodin,  or  other 
of  the  preparations  put  up  by  reputable  firms.  Personally  I 
have  never  yet  seen  a  patient  who  could  not  take  the  ordi- 
nar}^  iodides  in  some  form  or  other,  and  I  am  opposed  to 
ready  made  drugging. 


TREATALEXT  239 

The  action  of  the  iodides  is  to  lower  tlie  blood  pressure, 
and  they  are  of  ^'reatest  value  when  the  ])lood  pressure 
is  high,  and  when  headache  and  precordial  pain  are  present. 

When  the  case  is  moderately  advanced,  very  mild  doses, 
gr.  3/^,  morning  and  evening,  of  the  thyroid  extract  may  be 
given.  It  is  generally  believed  that  the  internal  secretion 
of  the  thyroid  and  the  adrenal  are  antagonistic.  That  the 
thyroid  secretion  lowers  blood  pressure  in  certain  forms  of 
hypertension  is  certain,  possibly  on  account  of  its  iodine 
content.  Some  combinations  of  iodine  and  thyroid  such  as 
the  iodothyroidin  have  been  used  and  have  had  some  meas- 
ure of  success  attributed  to  them. 

Hypertension  does  not  always  demand  active  measures 
for  its  reduction.  A^iewed  from  the  physiologic  stand- 
point, hypertension  is  but  the  expression  of  a  compensating 
mechanism  wiiich  is  designed  to  keep  the  blood  moving 
through  narrowed  channels.  Heart  hypertrophy  then  is 
al)solutely  essential  to  the  maintenance  of  life.  l{  has  ])een 
said  that  the  highest  blood  pressures  occur  in  chronic  dis- 
ease of  the  kidneys.  The  poisonous  substances  produced 
in  the  kidneys  must  exert  their  action  through  absorption 
into  the  general  blood  stream.  This  toxin  may  be  com- 
pletely eliminated,  if  we  accept  as  our  criterion  the  reduc- 
tion of  tension  to  normal  together  with  the  complete  return 
of  the  affected  individual  to  health.  A  concrete  example 
is  as  follows:  A  man  aged  44  years  was  brought  to  the 
^Milwaukee  County  Hospital  in  coma.  His  systolic  blood 
pressure  was  over  280  mm.  Hg,  diastolic  170  mm,,  his  urine 
contained  considerable  albumin  and  many  casts.  He  had 
general  anasarca.  Venesection  was  done  at  once  and  300 
c.c.  blood  obtained.  Immediately  following  this  operation 
the  pressure  was  210-150,  but  within  twelve  hours  it  was 
again  above  280-170.  He  was  given  no  medication  to  re- 
duce pressure  except  that  he  was  freely  purged.  He  was 
given  a  steam  sweat  bath  daily.  Frequent  blood  pressure 
readings  were  taken,    AVithin  seven  days  the  pressure  was 


240  ARTERTOSCLEROSTS 

130-86.  He  had,  in  the  meantime,  completely  recovered 
from  liis  symptoms.  ITe  was  kept  in  the  hospital  for  two 
weeks  longer  assisting  in  the  work  on  the  ward,  and  he  was 
discharged  with  a  pressure  (systolic)  between  130  and  136 
diastolic  80-84.  The  treatment  was  rest  in  bed,  free  purg- 
ing, venesection,  and  sweat  baths,  simple  but  exceedingly 
effective. 

Should  there  be  actual  indications  for  reducing  the  blood 
pressure,  I  must  admit  that  it  can  not  always  be  done.  The 
majority  of  cases  will  do  well  on  the  sodium  nitrite  or 
erythrol  tetranitrate.  However,  these  do  not  always  lower 
blood  pressure  and  keep  it  within  normal  limits.  When  a 
man  has  very  high  tension  we  do  not  wish  to  reduce  it  to 
what  it  should  normally  be  for  the  age  of  the  patient,  as 
symptoms  of  collapse  might  set  in  at  any  time  under  such 
conditions. 

Observations  made  with  the  sphygmomanometer*  show 
that  the  etfect  of  nitroglycerin  is  transient  or  of  no  effect 
except  in  doses  which  are  relatively  enormous  (one  drop  of 
the  one  per  cent  solution  given  every  hour).  Sodium  ni- 
trite may  lower  the  blood  pressure  but  the  etfects  will  have 
worn  off  in  two  hours.  It  is  the  same  with  erythrol  tetrani- 
trate. Sodium  sulphocyanate  in  doses  of  from  one  to  three 
grains  three  times  a  day  is  highly  recommended  by  some. 
My  own  experience  with  it  does  not  lead  me  to  believe  that  it 
is  of  any  great  value  in  hypertension.  It,  however,  may  be 
tried.  Benzyl  benzoate  has  been  used  recently  to  reduce 
the  high  blood  pressure  of  hypertension.  Macht  has  re- 
ported some  success.  In  the  author's  hands  it  has  been 
efficacious  in  a  few  cases.  As  long  as  the  patient  takes  the 
drug  the  pressure  may  be  slightly  reduced,  but  upon  the 
withdrawal  of  the  drug  the  pressure  returns  to  its  former 
level.    It  is  well  worth  a  trial  and  further  experimentation 


*Miller,  Jos.    L. :     Hypertension  and   the  V^alue  of  tlie  Various   Methods  for   Its   Re- 
duction.    Jour.  Am.  Med.  Assn.,  1910,  liv,  p.  1666. 


TREATMENT  241 

may  reveal  better  methods  of  administration.  The  dose  is 
from  2  to  6  c.c.  mixed  with  Avater  at  intervals. 

In  the  hypertension  of  tlie  menopause  some  have  had 
success  with  large  doses  of  corpus  luteum  extract.  As 
a  matter  of  fact  the  drug  treatment  of  hypertension, 
when  it  becomes  necessary  to  treat  this  condition  with 
drugs,  has  suffered  a  notable  set-back  since  more  careful 
control  has  been  made  with  tlie  blood  pressure  instruments. 
In  giving  any  of  the  depressor  drugs  their  action  should 
be  controlled  by  blood  pressure  measurements,  for  only 
in  this  way  can  we  be  sure  that  the  drug  is  exerting  its 
physiological  effect  and  we  may  expect  results.  The  indi- 
vidual reaction  to  these  drugs  varies  greatly  and  no  rule 
for  dosage  can  be  dogmatically  laid  down.  The  only  suc- 
cessful therapy  is  rigid  individualization.  This  is  the  key- 
stone to  treatment  in  cases  of  arteriosclerosis  and  high 
tension. 

It  must  not  be  inferred  from  what  has  been  said  that  the 
nitrites  are  of  no  value.  They  are  of  decided  value  but 
they  have  their  limitations.  The  most  evanescent  of  these 
drugs  is  amyl  nitrite.  This  is  put  up  in  the  form  of  cap- 
sules, or  pearls,  containing  from  one  to  three  minims.  AVlien 
it  is  desired  to  dilate  the  peripheral  vessels  suddenly,  one 
or  two  of  these  capsules  are  broken  in  a  clotli  held  to  the 
nose.  The  effect  is  almost  instantaneous.  There  is  flush- 
ing of  the  face  and  other  peripheral  vessels,  particularly 
near  the  head,  denoting  a  relaxation  and  widening  of  the 
bed  of  the  blood  stream,  and  a  consequent  decrease  in  pres- 
sure in  the  arteries.  These  effects  are  over  in  a  short 
while.  It  is  only  used  in  attacks  of  cardiac  spasm,  as  in 
angina  pectoris.  Nitroglycerin,  the  Spiritus  Glonoini  of 
the  U.  S.  P.,  acts  in  about  the  same  manner  as  amyl  ni- 
trite but  the  effects  last  usually  a  trifle  longer.  One  drop 
of  the  one  per  cent  solution  may  be  given  every  hour  until 
physiologic  effects  are  produced.  It  may  be  given  hypo- 
dermically.    This  may  be  a  means  of  reducing  pronounced 


242  ARTERIOSCLEROSIS 

liig'li  tension.  This  drug  has  l)een  found  of  benefit  espe- 
cially in  eases  where  arteriosclerosis  combined  with  chronic 
nephritis  causes  cardiac  asthma.  The  other  drug  which 
may  be  of  service  in  these  conditions,  one  whose  spliere 
of  action  is  somewhat  broader,  because  its  effects  are  more 
lasting,  is  sodium  nitrite.  This  is  given  in  water  in  doses 
of  one  to  three  or  five  grains  every  four  hours.  Some 
have  objected  to  the  use  of  this  drug,  but  my  experience 
has  made  me  place  considerable  confidence  in  its  harmless- 
ness,  provided  that  the  patient  is  carefully  watched.  This, 
however,  applies  to  all  of  the  nitrite  compounds.  My  ex- 
perience with  erythrol  tetranitrate  is  not  large.  It  may 
be  used  in  place  of  sodium  nitrite. 

For  a  mild  case,  one  often  finds  that  sweet  spirits  of 
niter  is  sufficient  to  control  tlie  pressure  and  relieve  the 
distressing  symptoms,  and  it  is  undoubtedly  the  least  harm- 
ful of  all  the  nitrites.  Drugs  that  are  of  great  value,  but 
of  which  little  is  noted  in  textbooks,  are  aconite  and  vera- 
truin  viride.  Both  of  these  drugs  are  well  known  to  be 
marked  circulatory  depressors.  Veratrum  viride  in  my  ex- 
perience should  be  very  cautiously  used,  and  never  used 
unless  a  trained  attendant  is  constantly  at  hand.  AVith  re- 
gard to  aconite  1  have  no  such  feeling,  and  a  mixture  of 
tincture  of  aconite  and  spiritus  etheris  nitrosi  ma}^  be 
given  for  several  weeks  with  no  fear  of  doing  any  harm. 
Personally,  of  all  the  drugs  mentioned,  I  prefer  the  nitrite 
of  sodium  or  the  combination  just  given.  They  may  be  ad- 
vantageously alternated. 

My  own  feeling  is  that  the  most  successful  means  of  treat- 
ment of  acute  high  tension  is  without  the  use  of  drugs. 
The  most  important  measure  is  absolute  rest  in  bed.  This 
often  suffices  to  lower  the  blood  pressure  and  to  arrest  the 
symptoms  produced  by  high  tension.  Venesection  I  believe 
is  also  of  value.  True  the  arterioles  appear  to  contract 
almost  immediately  upon  the  lessened  quantity  of  blood, 
or  there  is  immediate  interchange  of  serum  from  the  tissues 


treat:\iext  243 

^vhi('ll  l)ring's  the  l)l()()d  voluino  back  to  the  oi'i.giiial  amoiiiit. 
Whatever  happens  tlie  pressure  is  not  i>reatly  reclnced,  at 
times  not  reduced  at  all,  Init  often  tlie  symptoms  are  re- 
lieved. Hot  packs  or  sweat  l)aths  assuredly  do  reduce  the 
pressure  in  many  cases.  This  seems  to  me  to  be  an  ex- 
ceedingh^  valual)le  measure.  Finally  the  diet  should  be 
nourishing,  but  very  light,  not  too  nmch  fluid  should  be 
ingested,  and  the  bowels  should  l)e  freely  opened. 

With  the  fibrolysin  of  Merck,  I  have  had  no  experience. 
Some  men  assert  that  they  have  had  good  results  from 
its  use,  but  on  the  Avhole  the  evidence  is  not  highly  favor- 
able. 

iMorphine  is  invaluable.  No  drug  is  of  such  value  in  the 
nocturnal  dyspneic  attacks  that  occur  in  the  late  stages  of 
arteriosclerosis  when  the  heart  or  the  kidneys  are  failing. 
iMorphine  not  only  relaxes  spasm  and  quiets  the  cerebral 
centers,  but  is  an  actual  heart  stimulant  under  such  condi- 
tions, and  should  never  he  withheld,  as  the  danger  of  the 
patient's  becoming  addicted  to  its  use  is  more  fanciful  than 
j'eal.  However,  morphine,  at  times,  suppresses  the  secre- 
tion of  urine.  So  that  if  after  trial  the  urine  becomes 
scanty  and  the  edema  increases,  recourse  nuist  be  had  to 
other  drugs.  The  various  hypnotics  may  be  used  with 
caution.    One  which  seems  to  be  very  useful  is  adalin. 

As  heart  stinudants,  one  may  use  strychnine,  spartehi, 
caffein,  or  camphor.  In  desperate  cases,  where  a  rapidly 
diffusible  stimulant  is  needed,  a  hypodermic  syringeful  of 
ether  may  be  given,  and  repeated  in  a  short  while. 

Several  years  ago  a  so-called  serum  was  brought  out  by 
Trunecek  which  was  said  to  have  a  favorable  effect  on  the 
metabolism  of  the  vessel  Avails.  It  was  given  at  first  hypo- 
dermatically  or  intravenously  but  the  former  method  was 
])ainful.  It  was  later  stated  that  given  by  mouth  it  acted 
just  as  well.  The  results  with  the  Trunecek  serum  have  not 
come  up  to  the  expectations  that  the  early  favorable  reports 
promised.     The  original  sei'um  was  comjiosed  as  follows: 


244  APiTERTOSCLEKOSTS 

NaCl,  4.92  om.;  Na.SO.,  0.44  Rm.;  Xa.CO,,  0.21  o-m.; 
K,80,,  0.40  o-,n. ;  aqua  destil.  q.  s.  ad.  100.0  e.e.  Lator 
tliis  was  inodifKHl  for  internal  use  to  tlin  I'ollowiii^^  pro- 
scription : 

It      Natrii    clilor 10.       gm. 

Xatrii   suliiliat 1.       gm. 

Natrii  carboiiat O.-tO  gm. 

Natrii  phospliat 0.30  gm. 

Calcii  pliospliat. 

Magiiosii    pliospliat.    aa 0.75  gm. 

M.  Ft.  cachets  No.  XIII. 

The  contents  of  every  cachet  corresponds  to  15  c.c.  of  the 
fluid  serum  or  to  150  c.c.  of  blood  serum.  The  preparation 
called  antisclerosin  consists  of  the  salts  contained  in  the 
serum.  As  to  its  efficacy,  I  can  not  judge,  as  I  have  never 
felt  that  it  was  worth  Avliile  to  use  it.  Reports  of  cases  in 
which  it  has  been  tried  do  not  speak  very  highly  of  it. 

In  the  general  treatment  of  arteriosclerosis,  there  is  no 
one  factor  of  more  importance  than  the  regular  daily  bowel 
movement.  Attention  to  this  may  save  the  j)atient  nmcli 
discomfort  and  even  acute  attacks  of  cardiac  embarrass- 
ment. The  choice  of  the  purgative  is  immaterial,  with  tliis 
reservation  only,  that  the  mild  ones,  such  as  cascara,  rhu- 
barb, licorice  powder  and  the  mineral  waters,  should  be 
thoroughly  tried  before  we  resort  to  the  more  drastic  pur- 
gatives. Plenolphthalein  in  3  to  5  grain  doses  acts  remark- 
ably well  in  some  people  as  a  pleasant  laxative.  Agar-agar 
with  or  without  cascara  may  be  useful. 

Liquid  paraffin  under  a  variety  of  names  is  a  most  useful 
and  efficacious  laxative.  As  its  action  is  purely  mechanical 
it  may  be  taken  indefinitely  without  doing  harm  to  the  in- 
testinal musculature. 

The  old  Lady  AVebster  dinner  pill  is  an  excellent  tonic 
aperient.  AVhen  the  heart  is  embarrassed  and  edema  of  the 
legs  and  effusion  into  the  serous  cavities  have  taken  place, 
then  it  becomes  necessary  to  use  the  drastic  purgatives 
that  cause  a  number  of  watery  movements.     Epsom  salts 


TREATMENT  245 

given  ill  concentrated  form,  elaterin  gr.  1-12,  the  eoinpoiind 
cathartic  pill,  blue  mass  and  scammony,  or  even  croton 
oil  may  be  used.  Since  the  observation  of  a  greatly  con- 
gested intestine  from  a  patient  who  had  been  given  croton 
oil,  I  have  ceased  to  use  this  purgative,  and  I  doubt  much 
whether  its  use  is  ever  justifiable  in  these  cases. 

The  management  of  the  ordinary  case  of  arteriosclerosis 
resolves  itself  into  a  careful  hygienic  and  dietetic  regime 
with  the  addition  of  the  iodides,  aconite,  or  the  nitrites. 
A  diet  consisting  of  very  little  meat,  alcohol  in  moderation 
or  even  absolutely  prohi])ited,  and  not  too  much  fluid  should 
be  prescribed.  Condiments  and  spices  should  also  be  used 
sparingly.  Cold  baths,  shower  baths,  cold  and  hot  sheets 
alternating,  are  of  great  benefit  in  assisting  the  heart  to  do 
its  best  work  by  making  the  large  capillary  area  of  the  skin 
more  permeable.  It  is  not  true  that  such  liatlis  raise  the 
l)lood  pressure  so  markedly.  Certain  acts,  as  sneezing,  vio- 
lent coughing,  etc.,  increase  the  blood  pressure  much  more 
than  judicious  bathing. 

Symptomatic  Treatment 

The  fact  that  arteriosclerosis  really  loses  much  of  its  own 
identity  and,  in  later  stages,  becomes  merged  with  the  symp- 
tomatology of  the  diseases  of  various  organs,  as  the  kidney, 
brain,  heart,  compels  us,  for  completeness'  sake,  to  say  a 
few  words  aliout  the  treatment  of  these  complications. 

One  of  the  results  of  arteriosclerosis  of  the  coronary 
arteries,  angina  pectoris,  demands  prompt  treatment.  In 
the  acute  attack,  the  chief  object  is  to  relieve  the  spasm  and 
pain.  Pearls  of  amyl  nitrite  should  be  inhaled,  and  mor- 
phine sulphate  with  atropine  sulphate  given  hypodermat- 
ically  at  the  very  earliest  moment.  It  is  senseless  to  with- 
hold morphine.  The  only  possible  reason  for  withholding 
it  would  be  uncertainty  as  to  the  diagnosis.  It  is  probably 
better  to  err  on  the  safe  side,  and  should  the  case  prove  to 


246  AiiTKinoscLKito.sis 

1)0  one  ol'  ])s(>u(l()  angina,  in  the  next  attack  sterile  water 
can  be  given  instead  of  the  niori)hine  and  atropine. 

When  a  jiatient  is  seen  in  the  condition  of  broken  com- 
pensation with  the  nnich  dilated  heart,  anasarca,  dyspnea 
and  suppression  of  urine,  there  is  no  better  ])ractice  than 
venesection.  Es])ecially  is  this  valuable  when  the  tension  is 
still  fairly  high  and  the  individual  is  robust.  Following  the 
ahsti-action  of  six  to  eight  ounces  of  blood  (300-500  c.c,)* 
the  whole  picture  changes,  so  that  a  man  who  a  short  while 
before  was  apparently  at  death's  door,  notices  his  surround- 
ings and  takes  an  interest  again  in  life.  This  should  be  fol- 
lowed up  with  thorough  purgation,  and  cardiac  stimulants 
should  be  ordered.  In  such  cases  digitalis  is  useful,  but  its 
action  is  never  so  striking  as  in  cases  of  this  general  charac- 
ter due  to  uncompensated  valvular  disease.  It  must  be  re- 
membered that  in  arteriosclerosis  the  changes  in  the  myo- 
cardium must  be  of  a  considerable  grade  for  the  heart  to 
give  away.  Therefore,  digitalis  can  not  be  expected  to  act 
on  a  diseased  muscle  as  it  acts  on  a  comparatively  healthy 
muscle.  It  is  only  in  such  cases  of  broken  compensation 
that  digitalis  should  ever  be  used. 

Digitalis  is  not  a  general  vasoconstrictor  as  used  to  be 
taught.  Its  action  on  the  kidney  is  actually  a  vasodilator 
one.  And  in  its  action  on  the  heart  the  digitonin  dilates 
the  coronary  arteries,  according  to  Maclit,  while  the  digi- 
toxin  acts  on  the  heart  muscle.  Overdosing  wdtli  digitalis 
has  produced  partial  heart  block  in  many  cases.  It  is  ab- 
solutely contraindicated  in  Stokes-Adams  syndrome. 

There  are,  however,  some  cases,  especially  those  with 
transudations,  when  digitalis  may  be  carefully  tried  even 
though  high  tension  be  present.  It  is  simietimes  of  advan- 
tage to  combine  digitalis  with  the  nitrites  although  they  are 
said  to  be  i)hysi()l()gically  incompatible. 

Still  another  drug,  that  is  of  great  value  in  conditions  such 
as  have  been  described,  is  diui'etin.  This  may  be  given  in 
capsule  or  tablets,  grs.  x.  three  times  daily.     There  is  only 

*I  liMvc  taken  as  nnich  as  1700  c.c.  fniin  a  large  man.  lie  iccdvcrcil  and  went  l>ack 
to   work. 


TIIEATMEXT  247 

one  caution  to  express  in  the  use  of  tliis  drug-.  It  should  not 
be  given  when  the  kidneys  are  the  seat  of  chronic  inflam- 
matory changes;  in  fact,  actual  harm  may  be  done  by  ad- 
ministering the  drug  under  such  conditions. 

The  same  is  true  even  to  a  greater  extent  with  tlieocin. 
This  is  a  powerful  diuretic.  If  given  by  mouth  it  sliould  be 
well  diluted  as  it  is  most  irritating  to  the  stomach.  It  is 
best  given  intravenously  in  doses  of  two  and  a  half  to 
three  grains  dissolved  in  five  to  six  cubic  centimeters  of 
distilled  water.  One  must  be  reasonably  sure  that  the  kid- 
neys are  not  the  subject  of  chronic  disease  and  are  func- 
tionally, therefore,  below  par.  The  intravenous  dose  should 
not  be  given  oftener  than  once  in  four  days. 

For  the  pain  in  aneurysm,  nothing  (except,  of  course, 
morphine)  is  so  valuable  as  iodide  of  potassium.  Patients 
who  are  sutfering  agony,  when  ])ut  to  bed  and  given  KI 
grs.  X.  three  times  a  day,  soon  lose  all  the  distressing  symp- 
toms. This  applies  particularly  to  aneurysms  of  the  arch 
of  the  aorta. 

When  the  sclerosis  has  affected  the  cerebral  arteries  to 
such  an  extent  that  symptoms  result,  the  case  is,  as  a  rule, 
exceedingly  grave.  Not  much  can  be  done  except  to  relieve 
the  headaches  and  keep  down  the  blood  pressure,  if  this  is 
high,  by  means  of  rest  in  bed,  the  iodides,  aconite,  or  the 
nitrites.  The  cases  of  transient  monoplegias  or  ]iemij)legias 
can  be  much  relieved  by  careful  hygienic  measures  and  judi- 
cious administration  of  drugs.  ]\rucli  ingenuity  is  some- 
times required  to  overcome  the  idiosyncrasies  of  patients, 
but  care  and  patience  will  succeed  in  surmounting  all  such 
difficulties. 

The  treatment  of  intermittent  claudication  is  the  treat- 
ment of  arteriosclerosis  in  general.  Sometimes  the  circula- 
tion in  the  affected  leg  or  legs  is  much  helped  by  daily  warm 
foot  l)aths.  Light  massage  might  be  tried  and  the  galvanic 
current  mav  be  used  once  or  twice  dailv. 


248  ARTERTOSCLEROSIS 

There  are  a  few  distressing  symptoms  that  occur  usually 
late  in  the  disease,  when  complications  have  already  oc- 
curred, which  frequently  baffle  the  therapeutic  skill  of  the 
physician.  The  chief  of  these — insomnia,  dyspnea,  and 
headache — may  not  be  late  manifestations,  but  insomnia  and 
headache  are  frequently  associated  with  the  moderately 
advanced  stages  of  arteriosclerosis.  At  times  all  the  symp- 
toms seem  to  be  due  to  the  high  tension,  the  relief  of  which 
causes  them  to  disappear.  There  are,  unfortunately,  times 
when  high  tension  is  not  responsible  for  the  headache  and 
insomnia.  Under  these  circumstances  such  drugs  as  trional, 
veronal,  amylene  hydrate,  ammonol,  etc.,  may  be  tried  until 
one  is  found  which  produces  sleep.  For  the  headaches, 
phenacetin,  alone  or  in  combination  with  caffein  and  bro- 
mide of  sodium,  may  be  tried.  Acetanilid,  cautiously  used, 
is  at  times  of  value.  There  have  been  cases  of  arteriosclero- 
sis with  low  blood  pressure,  accompanied  by  severe  head- 
aches, that  have  been  relieved  by  ergot.  Codeine  should  be 
used  with  care,  and  morphine  only  as  a  ver}'  last  resource. 

Great  care  must  always  be  exercised  in  giving  drugs  that 
depress  the  circulation,  for  it  is  easily  conceivable  that  more 
harm  than  good  can  come  from  injudicious  drugging. 


CHAPTER  XIV 

ARTERIOSCLEROSIS  IN  ITS  RELATION  TO  LIFE 

INSURANCE 

The  value  of  the  early  recognition  of  cases  of  arterioscle- 
rosis and  hypertension  has  been  spoken  of  within,  but  it 
needs  to  be  further  emphasized.  There  is  perhaps  no  class 
among  physicians  to  whom  is  afforded  a  better  opportunity 
of  seeing  early  cases  than  the  medical  examiners  of  life 
insurance  companies. 

The  relationship  between  a  patient  and  the  physician 
whom  he  consults,  and  the  applicant  for  life  insurance  and 
the  examiner  are  diametrically  opposite.  In  the  former 
the  patient  desires  to  conceal  nothing  and  the  physician  is 
called  upon  to  diagnose  and  treat  disease.  In  the  latter  the 
applicant,  a  presumably  healthy  person,  may  have  much  to 
conceal  and  the  examiner  is  there  to  pass  upon  the  state  of 
health.  The  question  is  this — ''Is  the  applicant  now  in 
good  health  ? "  It  becomes  then  of  vital  importance  for  the 
examiner  to  be  able  to  detect  among  other  abnormal  condi- 
tions the  incipient  signs  of  arteriosclerosis  and  of  hyperten- 
sion. Parenthetically  it  may  be  stated  that  arteriosclerosis 
and  hypertension  are  not  one  and  the  same  disease  as  has 
been  so  frequently  insisted  upon  within;  the  former  may 
occur  without  the  latter  but  the  latter  can  not  from  its  very 
nature  be  present  for  long  without  arterial  thickening  su- 
pervening. It  is  necessary  in  discussing  the  question  here 
to  group  the  two  conditions  together  in  order  to  prevent 
needless  repetition. 

Such  a  case  as  the  following  is  common.  A  successful 
business  man  of  forty-four  years  was  brought  to  me  by  an 
agent  in  1905  for  examination.  The  man  was  six  feet  tall, 
weighed  218  pounds,  had  a  ruddy  color  and  looked  to  be  the 

249 


250  AHTKItlOSCLEItOSi!-; 

l)ictiire  ()[*  liealtli.  He  was  not  strictly  inteinperate,  ho 
never  ))e('aiue  intoxicated,  ])ut  every  day  he  drank  three  or 
four  wliiskies  and  often  he  had  a  bottle  of  wine  for  dinner 
in  the  evenin<>-.  When  he  was  examined  his  pulse  was  of 
good  quality  and  owing  to  the  fleshiness  of  the  wrist  it  was 
difficult  to  say  positively  whether  the  radial  artery  Avas 
sclerosed  or  not.  In  the  heart  no  nnirmurs  were  lieard,  and 
it  was  ditificult  to  be  sure  that  the  left  ventricle  was  enlarged. 
There  was,  however,  a  slight  ])ut  definite  accentuation  of  the 
second  sound  at  the  aortic  cartilage  which  might  readily 
have  been  overlooked  had  the  patient  not  been  stripped  and 
a  careful  examination  made  with  the  stethoscope.  Upon 
taking  the  blood  pi'essure  it  was  found  to  be  from  170-175 
nun.  of  Jig.  The  urine  specimen  examined  at  the  visit  was 
normal,  no  casts  were  found.  Tlui  applicant  was  seen  at 
his  home  and  the  blood  j^i'^'S^ure  measured.  It  was  again 
the  same.  He  was  seen  a  third  time  and  practically  the 
same  systolic  blood  pressure  was  found.  Under  protests 
from  all  the  agency  staff  the  man  was  declined.  Two  years 
later  he  died  of  apoplexy.  The  man  was  angry  at  being- 
refused.  Instead  of  looking  the  matter  squarely  in  the  face 
he  thrust  aside  the  idea  that  there  was  anything  the  matter 
with  him.  He  had  never  had  one  ill  day  in  his  life,  his  fore- 
l)ears  had  lived  to  ripe  old  age,  and  he  was  sure  that  he  knew 
more  about  himself  than  the  examiner. 

Had  this  applicant  showed  a  sense  of  reasonableness  he 
should  have  been  grateful  to  the  doctor  for  calling  his  atten- 
tion to  a  condition  which  surely  would  sooner  or  later  prove 
either  fatal  itself  or  lead  to  some  fatal  lesion.  It  Avas 
learned  that  this  man  had  gone  directly  to  his  family  physi- 
cian who  laughed  at  such  nonsense  as  had  ])een  told  the 
(now)  patient  by  the  examiner. 

Another  illustration  of  a  slightly  different  type  of  case  is 
afforded  in  the  following  history. 

A  inan  of  fifty  years  of  age,  five  feet  ten  in  height  and  104 
lbs.  in  weight,  was  brought  for  examination.    In  his  youth 


AKTERIOSCLEKOSIS    AND    LIFE    IXSUUAXt'E  251 

tliere  was  a  history  of  a  mild  attack  of  scarlet  fever.  He 
was  almost  a  total  abstainer,  rarely  taking  liciiior  in  any 
form.  Physically  lie  appeared  to  be  an  excellent  risk. 
However,  on  examining  the  heart  it  was  found  that  there 
was  slight  hyix'rtrophy  with  an  accentuated  second  aortic 
sound  at  the  base,  and  tlie  blood  pressure  was  180  mm.  of 
Hg.  Some  sclerosis  of  the  radial  arteries  was  found.  One 
comj)any  had  refused  him  on  account  of  albumin  in  the 
urine.  There  was  none  in  the  first  specimen  which  was 
passed  while  in  the  ofhc(^  The  specific  gravity  was  1014. 
A  morning  specimen  was  obtained  and  contained  a  trace  of 
albumin.  Sevei'al  s])ecimens  were  then  examined.  Some 
contained  albumin,  some  had  no  al))umin  content.  The  man 
was  declined;  no  protests  from  the  agent  as  albumin  had 
been  found.  There  was  something  tangible  in  that.  Had 
the  applicant  been  refused  on  account  of  his  high  tension, 
sclerosis  of  the  radials,  and  slightly  enlarged  heart  there 
would  undoubtedly  have*  been  protests.  And  yet  an  appli- 
cant revealing  such  a  state  of  the  cardiovascular  system 
without  albumin  in  the  urine  should  unhesitatingly  be  de- 
clined. Attention  has  been  called  to  hypertension  as  an 
early,  and  some  think  an  invariable,  sign  of  chronic  ne- 
phritis. My  own  experience  has  confirmed  me  in  the  belief 
that  in  hypertension  the  kidneys  are  often  the  seat  of 
chronic  interstitial  changes.  Careful  palpation  of  the  ra- 
dial and  l)rachial  arteries  will  in  every  case  reveal  more 
or  less  thickening. 

Tliere  is  yet  another  group  of  cases  which  the  examiner 
sees  as  healthy  subjects,  namely  those  cases  of  sclerosis  of 
the  peripheral  arteries  without  sclerosis  of  the  aorta  and 
without  high  tension.  In  such  cases  the  radials,  l)rachials, 
temporals  and  other  superficial  arteries  are  readily  palpa- 
ble, sometimes  even  revealing  irregularities  along  the 
course  of  a  vessel.  Such  cases  are  not  subj(H'ts  for  insur- 
ance. The  recognition  of  such  a  condition  is  of  great  impor- 
tance to  the  one  who  lias  it  and  he  should  be  uriicd  to  t>o  to 


252  ARTERIOSCLEROSIS 

liis  regular  physician  for  tlioroiigli  examination.  Should  the 
physician  ridicule  the  idea,  as  has  happened  to  me  more 
than  once  when  I  was  actively  engaged  in  insurance  work, 
the  examiner  has  done  his  full  duty  to  the  company,  the 
applicant,  and  himself. 

A  life  insurance  examiner  has  a  difficult  i)osition  to  fill. 
He  has  four  people  to  satisfy ;  the  applicant,  the  agent,  the 
medical  director  and  himself.  The  straight  and  narrow 
path  of  strict  honesty  is  his  only  salvation.  By  being  hon- 
est with  himself  he  necessarily  gives  a  scpiare  deal  to  the 
other  three  parties. 

No  applicant  who  has  palpable  arteries  or  hypertension 
can  be  considered  a  first  class  risk.  It  can  not  be  denied 
that  men  with  arteriosclerosis  live  to  an  advanced  age  and 
may  even  outlive  those  Avho  have  apparently  normal  ar- 
teries, but  the  average  life  expectancy  at  any  age  for  an 
arteriosclerotic  is  less  than  that  for  a  normal  person.  The 
apparently  healthy  applicant  who  learns  for  the  lirst  time 
when  examined  for  life  insurance  that  he  has  the  early  or 
moderately  advanced  signs  of  arterial  disease,  should  thank 
the  agent  and  examiner  for  showing  him  the  danger  signals 
ahead.  The  sensible  man  then  orders  his  life  so  that  he 
puts  as  little  strain  on  his  heart,  arteries,  and  kidneys  as 
possible  and  may  add  many  years  to  his  life. 

It  is  on  account  of  this  very  insidiousness  of  onset  that  I 
have  elsewhere  urged  as  a  prophylactic  measure  the  exam- 
ination every  six  months  of  all  persons  over  forty  years  of 
age.  I  am  more  and  more  convinced  that  it  is  of  vital  im- 
portance to  the  health  of  the  public. 

As  I  have  remarked,  the  average  man  consults  his  dentist 
at  least  once  a  year  so  that  no  tooth  may  be  so  far  diseased 
that  it  can  not  be  saved.  It  is  purely  a  means  of  preserving 
the  teeth.  "Why  not  do  the  same  with  the  whole  body?  Of 
what  use  is  it  to  save  the  teeth  and  lose  the  body?  It  seems 
to  me  that  the  great  army  of  life  insurance  examiners  are 
in  an  enviable  position  in  their  ability  to  add  years  of  life 


ARTEKTOSCLEROSTS   AND   LIFE    INSURANCE  253 

to  many  moii  and  Avomoii.  I  doubt  wliotlier  tlioy  roalize 
their  iniportanee  in  tlio  campaign  for  health.  I  shonld  urge 
life  insurance  companies  not  to  employ  recent  graduates 
unless  they  have  had  at  least  a  A'ear's  hospital  experience. 
For  the  company  as  well  as  for  the  individuals  I  l)elievo 
that  there  is  a  prognostic  sense  which  the  examiner  should 
have  and  this  can  only  be  acquired  by  experience. 

I  believe  that  arteriosclerosis  and  hypertension  are  in- 
creasing for  the  reasons  which  have  been  given  in  another 
chapter.  There  can  be  no  douljt  tliat  when  these  conditions 
are  recognized  long  before  symptoms  would  naturally  su- 
pervene, men  and  women  would  not  only  live  longer  l)ut 
also  die  more  comfortably  and  many  very  likely  would  l)e 
carried  off  by  some  disease  having  no  relationship  whatever 
to  arteriosclerosis.  Slight  enlargement  of  the  heart  down- 
ward and  to  the  left,  accentuation  of  the  second  aortic 
sound  at  the  base,  a  full  pulse,  arteries  which  are  palpably 
thickened,  increased  blood  pressure  are  signs  to  which  at- 
tention must  be  paid. 

AVhen  the  peripheral  arteries  are  palpable  they  are  not 
always  sclerosed.  The  radial  artery,  the  one  usually  pal- 
pated, may  lie  very  close  to  the  bone  in  a  thin  person.  Un- 
der these  conditions  the  artery  can  be  easily  felt.  It  is 
better  then  to  palpate  for  the  brachial  as  it  lies  beneath  the 
inner  edge  of  the  biceps  muscle.  Should  this  artery  be  felt 
then  very  probably  sclerosis  is  present.  Opinion  as  to 
whether  or  not  sclerosis  is  present,  when  it  is  slight,  may 
differ.  It  is  difficult  at  times  to  say  definitely.  Should 
such  be  the  case  the  applicant  should  be  most  carefully 
questioned  as  to  his  family  and  past  history,  the  heart 
should  be  carefully  outlined  by  percussion  and  the  blood 
pressure  should  be  taken,  both  the  systolic  and  diastolic 
pressures.  The  urine  should  be  examined  with  particular 
care.  I  am  aware  that  the  average  examination  for  life  in- 
surance is  not  made  with  the  care  which  is  bestowed  upon  a 
patient.    Yet  I  see  no  reason  why  the  same  attention  to  de- 


254  ARTKRIOSCLEROSIS 

tail  slioiild  not  Ix'  i>iv('n  in  oik^  as  in  the  other.  The  cxanii- 
iiation  ol'  tlie  ^roat  majority  ol'  a])i)li('aiits  can  bo  inade  in  a 
short  time,  as  there  is  no  qu(^stion  of  hitent  clironic  disease. 
When  the  exception  turns  up  lie  should  be  given  a  searchin*;- 
examination  and  a  full  i-eport  should  be  sent  to  the  Medical 
Director.  Only  in  this  ^vay  will  it  be  possible  to  weed  out 
the  luidesirable  risks. 

On  the  surface  it  does  not  seem  to  requii'e  any  g-i'eat  diag*- 
nostic  acumen  to  be  a  life  insurance  examiner.  In  the  old 
days  of  many  of  the  companies  there  were  no  examiners. 
The  applicant  was  br(mght  before  the  president  or  other 
appointed  official  and  Ik;  was  passed  or  rejected  on  his 
g-eneral  appearance.  This  has  changed,  and  now  the  med- 
ical department  with  its  scores  of  examiners  in  the  field  is 
a  well  organized  depai-tment. 

It  seems  to  me  that  the  examiner  should  be  an  exceedingly 
able  diagnostician  and  prognosticator.  There  is  no  telling 
when  he  may  be  called  upon  to  pass  judgment  on  a  border- 
line ease.  From  personal  experience  I  know  how  difficult 
it  is  to  make  a  decision  in  some  cases.  These  suspicious 
cases  after  a  careful  examination  had  better  be  passed  by 
the  examiner  and  a  supplementary  report  sent  to  the 
medical  director  containing  unbiased  details.  But  no  ap- 
plicant with  readily  palx)able  arteries,  even  though  the 
blood  pressure  l)e  normal,  should  l)e  considered  a  first  class 
insurance  risk. 

The  c{uestion  of  the  value  of  the  diasfolic  pressure  read- 
ing in  examinations  for  life  insurance  is  not  yet  settled  to 
the  satisfaction  of  all  medical  directors.  Certain  medical 
directors  with  clinical  experience  behind  them,  lay  great 
stress  on  the  increased  diastolic  pressure  and  consider  a 
persistent  diastolic  of  100  mm.  really  more  significant  as 
an  indication  of  hypertension  than  a  systolic  pressure  of 
1()0  mm.  Other  directors  pay  little  or  no  attention  to  the 
diastolic  reading.  Should  an  applicant  show  a  systolic 
above  the  average  normal  on  several  successive  readings, 


AnTERlOSCLEROSlS    AND    LIFE    INSURANCE  255 

he  is  declined.  AVlien  one  takes  into  consideration  tlic 
psychic  effect  of  knowing  that  he  is  being  examined  for 
high  l)h)od  pressure,  it  seems  unfair  to  refuse  insurance  on 
such  grounds  as  is  constantly  done. 

Up  to  the  present  there  are  no  extensive  series  of  life- 
expectancy  tables  in  which  hundrc^ds  of  thousands  of  cases 
are  analyzed  from  the  diastolic  pressure  values.  There  are 
many  such  tables  for  the  systolic  pressures  alone.  In  the 
tabulation  of  such  statistics  one  must  not  lose  sight  of  the 
important  fact  that  the  figures  are  taken  by  thousands  of 
men  of  varying  capacity  and  different  degrees  of  intelli- 
gence. Such  studies  to  be  of  any  real  value  must  be  taken 
from  records  made  at  the  home  offices  by  capable  men.  We 
shall  await  tliese  tables  with  interest.  In  tlie  meantime  Ave 
nuist  l)e  pei-mitt(Hl  to  have  the  impi'ession  that  the  diastolic 
pressure  has  l)een  nuich  neglected.  This  has  no  doubt  been 
due  to  the  difficulty  of  measuring  it  with  any  degree  of  ac- 
curacy. Now  with  the  auscultatory  method  and  the  correct 
place  to  read  the  diastolic  pressure  the  results  of  blood 
pressure  estimations  should  begin  to  have  some  value  for 
statistical  data. 

Clinically  the  diastolic  is  probably  more  important  than 
the  systolic.  Until  proof  is  brought  to  the  contrary  we  shall 
believe  tluit  in  life  insurance  examinations  it  has  the  same 
importance. 


CHAPTER  XV 

PRACTICAL  SUGGESTIONS 

The  time  spent  in  obtaining  a  careful  history  of  a  case 
is  time  well  spent.  Often  the  diagnosis  can  be  made  from 
the  history  alone,  the  physical  examination  merely  adding 
confirmation  to  the  data  already  obtained. 

The  younger  the  patient  who  has  arteriosclerosis,  the 
more  probable  is  it  that  syphilis  is  the  etiologic  factor. 
A  denial  of  infection  should  have  little  weight  if  the  history 
of  possible  exposure  is  present.  Miscarriages  in  a  woman 
should  arouse  the  suspicion  of  lues  in  her  husband.  The 
complement-fixation  reaction  will  often  clear  up  an  appar- 
ently obscure  diagnosis. 

There  are  various  ways  of  examining  a  patient  but  there 
is  only  one  right  w^ay;  the  examination  should  be  made  on 
the  bare  skin.  However  skillful  one  may  be  in  the  art  of 
physical  diagnosis,  he  can  gather  few  accurate  data  by  ex- 
amining over  the  clothes  even  if  he  use  a  phonendoscope. 

The  immoderate  eater  is  laying  up  for  himself  a  wealth 
of  trou])le  at  the  time  when  he  can  least  afford  to  bear  it. 
The  ounce  of  advice  in  time  is  worth  more  to  him  than  the 
pounds  of  medicine  later. 

It  is  a  wise  maxim  never  to  drive  a  horse  too  far.  Apply 
that  to  the  human  being  and  the  rule  holds  equally  well. 

There  may  be  no  symptoms  in  a  case  of  advanced  arterio- 
sclerosis. Do  not  on  that  account  neglect  to  advise  a  pa- 
tient in  whom  tlie  disease  is  accidentally  discovered. 

Many  a  man  owes  a  debt  of  gratitude  to  tlie  life  insurance 
examiner.    He  rarely  feels  grateful. 

When  a  competent  ophthalmologist  refers  a  case  to  a  gen- 
eral practitioner  with  the  statement  that  he  believes  from 
the  appearance  of  the  fundus  of  the  eye  that  arteriosclerotic 

256 


PRACTICAL   SUGGESTIONS  257 

changes  are  present  over  the  body,  the  case  should  be  most 
carefully  examined.  The  earliest  diagnoses  are  not  infre- 
quently made  by  the  ophthalmologist. 

It  is  the  part  of  wisdom  never  to  have  such  a  firmly  pre- 
conceived idea  of  the  diagnosis  that  facts  observed  are 
perverted  in  order  to  fit  into  the  diagnosis.  Let  the  facts 
speak  for  themselves. 

Beware  of  the  snap  diagnosis.  Even  in  a  case  of  well- 
marked  arteriosclerosis  when  the  diagnosis  seems  to  be 
written  in  large  letters  all  over  the  patient,  go  through  the 
routine.  Nine  times  out  of  ten  this  may  seem  needless. 
The  tenth  time  it  saves  your  conscience  and  reputation. 
Always  consider  that  you  are  examining  a  tenth  case. 

Grradual  loss  of  weight  in  a  person  over  fifty  years  old 
should  arouse  the  suspicion  of  arteriosclerosis. 

Do  not  call  the  nervous  symptoms  displa^^ed  by  a  middle- 
aged  man  or  woman  neurasthenia  until  you  have  ruled  out 
all  organic  causes,  particularly  arteriosclerosis. 

When  palpating  the  radial  artery,  always  use  both  hands 
according  to  the  method  already  described.  Pay  attention 
to  the  superficial  or  deep  situation  of  the  artery. 

The  examination  of  one  specimen  of  urine  does  not  give 
much  information,  especially  if  it  should  be  found  to  con- 
tain no  abnormal  elements.  Fairly  accurate  data  may  be 
gathered  from  the  mixed  night  and  morning  urine;  most 
accurate  data  from  the  twenty-four  hour  specimen.  To  be 
of  any  real  value  there  should  be  frequent  examinations  of 
the  day's  excretion. 

In  measuring  the  day's  output  a  good  rule  is  as  follows: 
begin  to  collect  urine  after  the  first  morning's  micturition 
and  collect  all  including  the  first  quantity  passed  the  next 
morning.  It  is  best  to  examine  the  centrifugated  urine  for 
casts  even  though  no  albumin  be  present.  It  is  useless  to 
look  for  casts  in  an  alkaline  urine. 

Casts  are  not  infrequently  found  in  chemically  normal 
urine  from  a  middle-aged  patient.    Other  things  being  nor- 


258  ARTERIOSCLEROSIS 

mal,  the  finding  has  no  significance.    The  kidneys  must  be 
carefully  tested  functionally. 

Blood  pressure  readings  should  always  be  taken  with  the 
patient  in  the  same  posture  at  every  estimation.  At  the 
first  examination  it  is  advisable  to  take  readings  from  both 
brachial  arteries.  Let  the  patient  sit  comfortably  and  relax 
all  muscles. 

Differentiate  as  soon  as  possible  between  the  uncom- 
pensated heart  caused  by  valvular  disease  and  that  caused 
by  arteriosclerosis.  There  is  a  difference  in  prognosis. 
Both  give  the  same  symptoms,  and  are  treated  similarly  un- 
til compensation  returns ;  thereafter  the  management  of  the 
two  forms  is  different. 

Aortic  incompetence  that  comes  on  late  in  life  is  gener- 
ally the  result  of  curling  of  the  free  margins  of  the  valves 
caused  by  syphilitic  arteriosclerosis.  Prognosis  is  grave 
because  of  the  fact  that  the  heart  muscle  also  is  the  seat  of 
degenerative  changes  and  compensatory  hypertrophy  is  es- 
tablished with  difficulty. 

When  laying  down  a  regime  for  a  patient,  consider  his 
disposition,  and  individualize  the  treatment.  Kemember 
that  exercise  is  an  essential  feature  of  the  hygiene  of  the 
patient's  life  but  do  not  forget  to  be  explicit  about  the 
amount  and  character  of  the  permissible  exercise. 

In  the  prophylaxis  of  arteriosclerosis,  a  rational  mode  of 
living  is  the  all-important  factor.  As  a  rule,  the  less  meat 
one  eats,  the  less  is  the  liability  of  arterial  degeneration  as 
age  advances.  The  exceptions  to  this  rule  are  many,  and 
probably  depend  upon  the  character  of  the  ''vital  rubber" 
with  which  the  individual  begins  life. 

The  diet  in  well-marked  cases  of  arteriosclerosis  should 
be  carefully  selected  with  regard  to  its  nutritive  and  non- 
irritating  character.  Animal  proteins  should  be  sparingly 
used.    Milk  should  have  an  important  place  in  the  dietary. 

No  drug  relieves  the  pain  of  uncomplicated  aneurysm  as 
surely  as  iodide  of  potassium. 


PRACTICAL    SUGGESTIONS  259 

Iodides  frequently  upset  the  stomach.  Be  cautious  in  the 
use  of  them.  The  irritable  stomach  may  turn  the  scales 
against  your  patient. 

Use  cardiac  stimulants  with  care  and  judgment.  If  all 
the  valuable  ammunition  is  used  up  at  first,  the  fight  will  be 
lost. 

Use  digitalis  with  especial  care.  Its  chief  usefulness  is 
in  steadying  the  decompensated  heart,  improving  the  con- 
duction of  impulses,  and  increasing  the  tone  of  the  cardiac 
muscle.  It  should  never  he  given  to  patients  with  very  sloiv 
pulses,  the  subjects  of  Stokes-Adams  syndrojne.  Digitalis 
has  been  found  to  produce  partial  to  complete  heart  block 
when  therapeutically  administered. 

Eemember  that  in  the  uncompensated  heart  morphine  not 
only  eases  the  oppressive  dj^spnea,  but  also  steadies  and 
stimulates  the  heart. 

See  to  it  that  the  patient  has  a  daily  movement  of  the 
bowels.  In  the  early  stage  try  the  effect  of  liquid  paraffin 
or  of  the  mineral  waters  such  as  Pluto,  or  Huiwadi  Janos, 
or  artificial  Carlsbad  salts  (Sprudel  salts).  These  last  can 
be  made  as  follows :  Sodium  chloride,  oi ;  sodium  bicarl)0- 
nate,  .3I1 ;  sodium  sulphate,  .jiv.  Take  two  tablespoonsf ul  of 
this  in  a  glass  of  hot  water  before  breakfast.  Should  these 
not  succeed,  assist  the  action  of  the  drugs  by  the  use  of 
enemata.  The  pill  of  aloin,  strychnine  sulphate,  and  extract 
of  cascara,  with  the  addition  of  a  small  quantity  of  hyoscy- 
amus,  is  a  mild  tonic  purgative.  In  cases  of  constipation 
with  high  tension,  there  is  no  drug  as  valuable  as  calomel  or 
one  of  the  other  mercurials  given  occasionally. 

Never  give  Epsom  salts  unless  copious  watery  stools  are 
desired  to  deplete  effusion  into  the  serous  cavities  or  into 
the  subcutaneous  tissue. 

Chronic  constipation  increases  the  gravity  of  the  prog- 
nosis. 

In  case  of  suppression  of  urine  and  anasarca,  hot  air 
packs  may  be  of  value.    The  patient  may  ])e  wrapped  in  a 


260  ARTERIOSCLEROSIS 

hot  wet  sheet  and  covered  with  blankets.  I  do  not  believe  in 
administering  pilocarpine  to  assist  the  sweating. 

Remember  to  treat  the  patient  and  not  the  disease.  The 
careful  hygienic  and  dietetic  treatment,  combined  with  the 
least  amount  of  drugging,  is  the  best  and  most  rational 
method  of  treatment. 


INDEX 


A 

Abdominal   symptoms,  201 
Aconite  in  treatment,  242 
Acquired  arteriosclerosis,  159 
Adami,  effect  of  syphilis  in  aorta,  45 
Adventitia,   28 
Age  in  arteriosclerosis,  161 
Albuminuria,  221 

Albutt  's   classification    of   arterioscle- 
rosis, 186 
Alcohol,  166,  228,  235 
Anatomy,  25 
Angina  abdominalis,  201,  216 

pectoris,  197,  216 
pseudo,   216 
Angioselerosis,  26,  64 
Aorta,  27 

anatomical  lesions  in,  33 

Aschoff  on,  35 

normal,  41 

syphilis  in,  44 

thoracic,  29 

thoracic     and     abdominal,     arterio- 
sclerosis of,  39 

velocity  of  blood  in,  66 
Aortic  incompetence,  61,  258 

stenosis,  60 
Aortitis,  acute,  165 
Arcus  senilis,  191 
Arrhythmia,  tonal,  92,  102 
Arterial  pressure,  85 

symptoms,  189 
Arteries,  29 

examination  of,  172,  177 

general  structure  of,  27 

large,  30 

adventitia  of,  30 

palpable,  189 

pulmonary,  arteriosclerosis  of,  63 
Arteriocapillary   fibrosis,   26 
Arteriosclerotic   endocarditis,   60,   219 
Artery,  coronary,  cross-section  of,  36 

pulmonary,  209 

radial,  29 
Aschoff  on  aorta,  35 
Atheroma,  simple,  32 
Atheromatous  abscess,  38 
Auricular  fibrillation,  133 

flutter,  131 
Auscultation,  176 


Auscultatory  blood   pressure  phenom- 
enon, 90 
method  of  taking  Ijlood  pressure,  83 
percussion,  175 

B 

Balneotherapy,  233 

Basch's  blood  pressure  instrument,  70 
Blood,  circulation  of,   63 
velocity  of,  65 
in  animals,  66 
in  aorta,  66 
in  capillaries,  66 
viscosity  of,  68 
Blood  pressure,  68 

auscultatory    method    of    taking, 

83 
clinical    applications    of,    147 
diurnal  variations   of,   102 
drugs  influencing,  120 
estimation  of,  179 
in  cancer,  118 
in  collapse,  118 
in  exercise,  105 
in  head  injuries,  148 
in  hemorrhages,  105,  118,  148 
in   infectious   diseases,    153 
in  kidney  diseases,  155 
in  meningitis,  118 
in    obstetrics,   152 
in  j)ulmonary  tuberculosis,  119 
in  shock,  105,  148 
in  surgery,  147 
in  typhoid  fever,  118,   154 
in  valvular  heart  disease,  155 
increase  of,  55 
instruments,  70 

Brown's,  74 

Cook's,  71 

Erlanger's,  72 

Faught's,  75,  80 

Hill  and  Barnard 's,  70 

Hirschfelder  's,  73 

K.  Vierordt's,  70 

Marey's,  70 

Potain's,  70 

Eiva  Rocci  's,  70 

Roger's,   77 

Sanborn's,   80 


261 


262 


INDEX 


Blood  ])rossuro  instruments — Cont  'd. 
Stanton's,  72 
technique  of,   80 
"Tyeos,"  77 
V.  Basch's,  70 
V.  Recklinghausen 's,  76 
mechanism  of,  55 
normal  variations  of,  88 
])henomenon,   auscultatory,   90 
])recautions  when  estimating,  181 
value  of,  181 
Bowman's  capsules,   sclerosis   of,   62 
Brain,  changes  in,  62 
Brown  atrophy,  60,  118,  201 


Calcification  of  media,  43,  59 
Cancer,  blood  pressure  in,  118 
Capillaries,  anatomy  of,  27^  31 
Capillary    ])ulse,    67 
Cardiac   dullness,   172 

irregularities  in  arteriosclerosis,  131 

symptoms,  195 
Cerebral  symi)toms,  203 
Circulation  of  Idood,  65 

physiology    of,    65 
Cirrhosis  of  liver,  64,  216 
Classification    of    arteriosclerosis,    32, 
37 
Allbutt's,  186 
Collapse,  l)lood  pressure  in,  118 
Congenital   arteriosclerosis,    157 
Cook's  blood  pressure  instrument,   71 
Cor  bovinum,  116 

Coronary  artery,  cross  section  of,   36 
Corpus  luteum,  241 


D 


Definition  of  arteriosclerosis,  26 
Diabetes  mellitus,  216 
Diagnosis,  210 

differential,  215 

early,  210 

ophthalmic  examination  in,  214 
Diastolic  pressure,  69,  83,  85,  94 

importance  of,   97 
Dicrotic   pulse,   123 
Dietetic  treatment,  235 
Differential   diagnosis,   166,   215 
Diffuse  arterioclcrosis,  32,  37,  38,  57 
Digitalis  in  treatment,  246,  259 
Diuretin  in  treatment,  246 
Drug  intoxications,   166 
Drugs  influencing  blood  pressure,  105 

120 
Ductless  glands,  171 


Dullness,  cardiac,  172 
Dyspeptic    symptoms,    184 
Dyspnea,  184 

treatment  of,  248 

E 

Electrocardiogram,  126 
Embolism,  59 
Endarteritis  deformans,  47 

o])literans,  46 
Endocarditis,  arteriosclerotic,  60,  219 
Endothelial   lining,    27 

tubes,  31 
Epistaxis,  184,  221 
Erlanger  's  blood  pressure  instrument, 

72 
Erythromelalgia,  192,  208 
Estimation  of  blood  pressure,  179 
Etiology,  157 
Examination  of  arteries,  172,  177 

of  heart,  172 

of  urine,  257 
Exercise,  blood  pressure  in,  105 

in  prophylaxis,  225 

in  treatment,  230 
Experimental  arteriosclerosis,  50 
Extrasystole,   138 


Faught's    blood    pressure    instrument, 

75,  80 
Fibrillation,  auricular,  133 

ventricular,  138 
Fibrolysin    in   treatment,    243 
Fingernail   palpation,   178 
P"'inger  tip  palpation,  179 
Flutter,   auricular,   131 
Food  poisons  in  arteriosclerosis,  163 


G 


Gibson 's  law,  154 

H 

"H"  wave,  126 

Habits,  personal,  234 

Head  injuries,  blood  i>ressure  in,  148 

Headache,  184 

treatment  of,  248 
Heart   block,   140 

boundaries,  172 

examination  of,  172 

hypertrophy  of,  60 

physical  examination  of,  172 

stimulants,  243,  246,  259 

symptoms,  188 


INDEX 


263 


Hemorrhages,  blood  pressure  in,  118 
Henle,  membrane  of,  29 
Hill  and  Barnard's  blood  pressure  in- 
strument, 70 
Hi rschf elder 's   ])lood   pressure   instru- 
ment, 73 
His,  bundle  of,  141,  197 
Hygienic  treatment,  230 
Hyperpietic  arteriosclerosis,  186 
Hypertension,  60,  106,  169,  185,  249 

cause  of  arteriosclerosis,  159 

classification  of  cases,  112 
Hypertrophy  of  left  ventricle,  58 
Hypotension,  117 


Incompetence,   aortic,   61,   258 
Indicanuria,   167 
Infants,   arteriosclerosis  in,   158 
Infectious  diseases  in  arteriosclerosis, 
163 

blood  pressure  in,  153 
Insomnia,  treatment  of,  248 
Intermittent  claudication,  192,  208 

treatment  of,  247 
Intoxications,  chronic  drug,  166 
Intracranial  tension,   105 
Involutionavy  arteriosclerosis,   187 
Iodides  in  treatment,  238,  247,  259 

K 

Kidney  diseases,  blood  pressure  in,  155 
Kidneys,  sclerosis  of,  61,  170 


Life  insurance,  relation  to,  249 
Light  percussion,  174 

touch  palpation,  175 
Liver,  cirrhosis,  64,  216 
Local  symptoms,  207 

M 

Marey's  blood  pressure  instrument,  70 
Maximum  pressure,  85,  94 
Mean  pressure,  85 
Media,  calcification  of,  43,  59 
Medicinal  treatment,  238 
Meningitis,  lilood  pressure  in,  118 
Mental  strain,  168 
Mesaortitis,  45,  47,  49,  165 
Mesentery,  cross-section   of  small   ar- 

tcrv  in,  56 
Milk  diet,   237 
Minimum  pressure,  86,  94 


Moenckeberg  type  of  arteriosclerosis, 

43 
Morphine  in  treatment,  243 
Mosenthal  test  meal,  221 
Muscular  overwork,  169 


N 


Xervous  symptoms,  191 
Xitrites  in  treatment,  240 
Xitroglycerin  in  treatment,  241 
Xodular  arteriosclerosis,  32,  37 
Xormal  blood  pressure  variation. 


O 


Obstetrics,  blood  pressure  in,  152 
Occupation  in  arterioclerosis,  162 
Ocular  symptoms,  190 
Ophthalmic    examination,    importance 
in  early   diagnosis,  214,   256 
Orthodiagraph,  173 
Over-eating,  167,  212,  225,  235. 
Over-work,  muscular,  169. 


"P"  wave,  129 
"P-R"  interval,  130 
Palpable  arteries,  189 
Palpation,  174,  180 

fingernail,   178 

finger  tip,  179 

light  touch,  175 
Pathology,  32 
Percussion,  174 

auscultatory,  175 

light,  174 
Peripheral  symptoms,  207 
Personal  habits,  234 
Phlebosclerosis,  64 
Phthalein  test,  221 
Physical  signs,  183 
Physiology   of  the   circulation,   65 
Potain's  blood  pressure  instrument,  70 
Practical  suggestions,   256 
Pressure,  arterial,  85 

ausculatorv  method  of  determining, 
83  " 

diastolic,   83,  94 

estimation  of,  179 

in  surgery,  147 

maximum,  85,  94 

normal  variations,  88 

pulse,  83,  85,  87,  100         ' 

systolic,  82,   85 

technique,  80 

venous,  120 


264 


INDEX 


Prognosis,    23  8 
Prophylaxis,  224 

exorcise  in,  225 
Pseiulo  angina  pectoris,  216 
Pnlmonary  artery,  209 
arteriosclerosis  of,  63 

tuberculosis,  l)loo(l  pressure  in,  119 
Pulse,   123 

capillary,  67 

deficit,  135 

dicrotic,   123 

in   arteriosclerosis,   123 

pressure,  69,  83,  85,  87,  100 

rate,  69 

venous,  123 
Purgatives  in  treatment,  244,  259 
Pyrosis,   184 


Q 


Q  E  S"  complex,  129 


E 


Rabbits,   lesions   produced   experimen- 
tally in,  50 

Race  in  arteriosclorosis,  161 

Radial  artery,  29 

Radials,  sclerosis  of,  43 

Raynaud's  disease,  192,  207 

Recklinghausen 's    blood    pressure    in- 
strument, 76 

Renal  disease,  169 
symptoms,   199 

Rest  in  treatment,  242 

Riva-Rocci's    blood    pressure    instru- 
ment, 70 

Rogers'  blood  pressure  instrument,  77 


Sanborn's  blood  pressure  instrument, 

80 
Scaphoid  scapula,  158 
Schwellungsperkussion,  174 
Sclerosis  of  veins,  64 
Senile  arteriosclerosis,  32,  37,  43,  59 
Sex  in  arteriosclerosis,  161 
Shock,  blood  pressure  in,  105,  148 
Spinal  symptoms,  205 
Spirochaeta  pallida,  45 
Stanton's  blood  pressure  instrument, 

72 
Stenosis,  aortic,  60 
Stokes-Adams  syndrome,  197 
Stomach,  ulcer  of,  216 
Strain  hypertrophy,  47,  54,  55 
Surgery,  blood  pressure  in,  147 


Symptomatic  treatment,   245 
Symptoms,  183 

abdominal,  201 

arterial,  189 

cardiac,  195 

cerebral,  203 

dyspeptic,  184 

dyspnea,  184 

general,  183 

headache,  184 

heart,   188 

local,  207 

nervous,  191 

ocular,  190 

peripheral,  207 

pyrosis,  184 

renal,  199 

special,  194 

spinal,  205 

vertigo,  184 

visceral,  201 
Syphilis,  165 

in  aorta,  44 
Syphilitic  arteriosclerosis,  37 
Systolic  pressure,  69,  82,  85,  94 

importance  of,  97 


T 


"T"  wave,  130 

Technique    of    blood    pressure    instru- 
ments, 80 
Thayer  and  Fabyan,  34 
Theocin,  247 

Thoma  on  arteriosclerosis,  33 
Thoracic  aorta,  29 
Thyroid  extract  in  treatment,  239 
Tobacco,  167,  212,  234 
Tonal  arrhythmia,  92,  102 
Toxic  arteriosclerosis,   186 
Treatment,  229 

aconite  in,  242 

balneotherapy  in,  233 

corpus  luteum,  241 

dietetic,   235 

digitalis  in,  246,  259 

diuretin  in,  246 

exercise  in,  230 

fil)rolysin  in,  243 

lieart  stimulants  in,  243 

hvgienic,    230 

iodides  in,  238,  247,  259 

medicinal,   238 

morphine  in,  243 

nitrites  in,  240 

nitroglycerin  in,  241 

of  dyspnea,  248 

of  headache,  248 


INDEX 


2G5 


Treatment — Cont  'd. 

of  insomnia,  248 

of  intermittent  claudication,  247 

personal  habits  in,  234 

purgatives  in,  244,  259 

rest  in,  242 

symptomatic,    245 

theocin  in,  247 

thyroid  extract  in,  239 

Trunecek's   serum  in,   243 

venesection  in,  242 

veratruni  viride  in,  242 
Trunecek's  serum  in  treatment,  243 
Tuberculosis,  blood  pressure  in,  119 
Tunica  intima,  28 

media,  28 
' '  Tycos ' '   blood   pressure   instrument, 

77 
Typhoid    fever    as    cause    of    arterio- 
sclerosis, 164 
blood  pressure  in,  118 


U 

Ulcer  of  stomach,  216 
Urine,  examination  of,  257 
suppression  of,  259 


Valvular  heart  disease,  blood  pressure 

in,  155 
Vasa  vasorum,  29 
Veins,  anatomy  of,  30 

sclerosis  of,  64 
Velocity  of  blood  in  animals,  66 

of  blood  in  aorta,  66 
Venesection  in  treatment,  242 
Venous  pressure,  120 

pulse,  123 
Ventricle,  left,  hypertrophy  of,  58 
Ventricular   fibrillation,    138 
Veratruni  viride  in  treatment,  242 
Vertigo,  184 


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